Publications by authors named "Hüseyin Serkan Erol"

24 Publications

  • Page 1 of 1

(1 → 3)-β-d-glucan enhances the toxicity induced by Bortezomib in rat testis.

J Food Biochem 2020 03 20;44(3):e13155. Epub 2020 Jan 20.

Department of Urology, Faculty of Medicine, Aksaray University, Aksaray, Turkey.

We aimed to determine the possible effects of the antioxidant agent (1 → 3)-β-D-glucan on bortezomib-induced rat testis damage. We used five groups of rats; control, (1 → 3)-β-D-glucan (75 mg/kg), bortezomib group, bortezomib + (1 → 3)-β-D-glucan groups (injection of (1 → 3)-β-D-glucan after bortezomib and sacrificed at 48th or 72nd h). The effects of these substances were assessed by measuring the levels of the antioxidant enzymes and LPO, and by performing immunohistochemical analysis with NF-κB. The histology of testis was evaluated using aniline blue staining. (1 → 3)-β-D-glucan leads to significant reductions in the levels of antioxidant enzymes and increased levels of LPO in testes. Moreover, it increased the NF-κB immunopositivity significantly in testis, especially in Bortezomib + (1 → 3)-β-D-glucan group at 48th h. The histological changes were observed in the bortezomib and/or (1 → 3)-β-D-glucan groups. Our results demonstrated that testis damage caused by the treatment with bortezomib was not eliminated by (1 → 3)-β-D-glucan and shockingly it increased the damage. PRACTICAL APPLICATIONS: The testis damage caused by the treatment with bortezomib was not eliminated by (1 → 3)-β-D-glucan and as a result, β-1,3-(D)-glucan enhanced the toxicity by leading a decrease in the levels of GSH, SOD, and CAT, thus caused an elevation in the immunoreactivity of NF-κB and altered the histopathological changes by enhancing the toxic effects of bortezomib. The findings of the previous studies about the antioxidative activity of (1 → 3)-β-D-glucan are controversial. So, it is necessary to consider the cytotoxicity of (1 → 3)-β-D-glucan in testis tissue. Thus, more studies on testis tissue are necessary to confirm that (1 → 3)-β-D-glucan is safe as an antioxidant.
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http://dx.doi.org/10.1111/jfbc.13155DOI Listing
March 2020

The propolis and boric acid can be highly suitable, alone/or as a combinatory approach on ovary ischemia-reperfusion injury.

Arch Gynecol Obstet 2019 11 23;300(5):1405-1412. Epub 2019 Sep 23.

Department of Pathology, Faculty of Veterinary Medicine, Ataturk University, Erzurum, Turkey.

Purpose: Ovarian ischemia-reperfusion (IR) damage continues to be a serious infertility problem. The oxidative stress plays central role in the development of IR injuries. Activation of antioxidants decreases IR injuries; however, the efficacy of antioxidant agents remains controversial. Unfortunately, there has been no evidence for medicinal use of boric acid (BA) and propolis (Prop) on ovarian IR injury on rats so far. This study will provide to reveal the potential applications of the Prop and BA in ovarian IR therapy.

Methods: The Sprague-Dawley rats were randomized into five groups: I-control, II-IR, 3 h of ischemia and 3 h of reperfusion, III and IV-a signal dose of oral BA (7 mg/kg) and Prop (100 mg/kg) alone 1 h before induction of IR, V-Prop and BA together 1 h before induction of IR. SOD (superoxide dismutase), CAT (catalase), GSH (glutathione), MPO (myeloperoxidase), MDA (malondialdehyde), and IL-6 (interleukin-6) levels were quantified by ELISA and the TNF-α (tumor necrosis factor-α), 8-OHdG (8-hydroxylo-2'-deoxyguanosin) and Caspase-3 expressions were performed by immunohistochemical analyses.

Results: BA and Prop pretreatment significantly reduced MPO, MDA, and IL-6 levels and pathologic score in IR rats, with no effects in control group. These agents used in therapy also decreased TNF-α, 8-OHdG and Caspase-3 protein expressions increased by IR. Furthermore, BA and Prop combination showed significant ameliorative effects on ovary injury caused by IR through acting as an antioxidant, anti-inflammatory and antiapoptotic agent.

Conclusion: BA and Prop alone and especially in combination could be developed as therapeutic agents against ovary IR injury.
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http://dx.doi.org/10.1007/s00404-019-05303-9DOI Listing
November 2019

Evaluation of the Roflumilast Effect Supplemented with Linezolid in Pleural Empyema in Rats Caused by Intrapleural Staphylococcus aureus Inoculation.

Jpn J Infect Dis 2020 Jan 30;73(1):1-7. Epub 2019 Aug 30.

Department of Pulmonary Diseases, Ataturk University School of Medicine.

In addition to tube drains, pleural empyema is treated with antibiotics and anti-inflammatory drugs. We aimed to evaluate the anti-inflammatory activity of roflumilast combined with linezolid in a rat model of pleural empyema induced by Staphylococcus aureus. A total of 40 rats were divided into 7 groups: sham (n = 4), S. aureus inoculation (n = 6), S. aureus + 10 mg/kg linezolid (n = 6), S. aureus + 5 mg/kg roflumilast (n = 6), S. aureus + 10 mg/kg linezolid + 5 mg/kg roflumilast (n = 6), S. aureus + 10 mg/kg roflumilast (n = 6), and S. aureus + 10 mg/kg linezolid + 10 mg/kg roflumilast (n = 6). Animals were administered linezolid 1 h before and 12 h after inoculation with S. aureus. Roflumilast was administered orally as a single dose 30 min before inoculation with S. aureus. Compared to linezolid treatment alone, linezolid combined with 5 mg/kg roflumilast significantly improved TNF-α, IL-1β, vasodilation/congestion, and tissue/pleural polynuclear leukocyte (PNL) infiltration (p < 0.05). Linezolid combined with 10 mg/kg roflumilast also provided a significant improvement in TNF-α, IL-1β, IL-6, endothelin-1, vasodilation/congestion, mesothelial cell damage, lung tissue PNL, and pleural PNL compared to linezolid alone (p < 0.05). Due to its anti-inflammatory effects and significant impact on recovery, roflumilast can be used in conjunction with antibiotherapy for the treatment of pleural empyema.
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http://dx.doi.org/10.7883/yoken.JJID.2019.164DOI Listing
January 2020

The Protection Potential of Antioxidant Vitamins Against Acute Respiratory Distress Syndrome: a Rat Trial.

Inflammation 2019 Oct;42(5):1585-1594

Faculty of Veterinary Medicine, Department of Biochemistry, Ataturk University, 25100, Erzurum, Turkey.

Acute respiratory distress syndrome (ARDS) is a fatal disease that includes inflammation formed by septic and non-septic causes. Reactive oxygen radicals (ROS) play a key role in ARDS pathophysiology and constitute the base of damage process. Antioxidant vitamins are used for inhibiting hazardous effects of radicals. Therefore, effects of antioxidant vitamins such as α-lipoic acid (ALA), vitamin E (VITE), and C (VITC) were investigated on oleic acid (OA)-induced ARDS rat model. Furthermore, high and low dose of methylprednisolone (HDMP, LDMP) was used for comparing effects of the vitamins. In this study, 42 male rats were divided to seven groups named control, OA, ALA, VITE, VITC, LDMP, and HDMP. OA was intravenously administered to all groups except control group and other compounds were orally administered (ALA, VITE, and VITC: 100 mg/kg, LDMP: 5 mg/kg, HDMP: 50 mg/kg) after OA injections. OA increased MDA level in lung tissue and TNF-α and IL-1β cytokine levels in serum. ALA, VITE, VITC, and both dose of MP significantly decreased the cytokine levels. Although OA reduced SOD, CAT, and GSH levels in lung tissue, the vitamins and LDMP markedly enhanced the levels except for HDMP. Furthermore, OA showed thickening in bronchi and alveolar septum, hyperemia in vessels, and inflammatory cell infiltrations in lung tissue histopathological examinations. Antioxidant vitamins may be useful for premedication of ARDS and similar disorders. However, methylprednisolone was not found sufficient for being a therapeutic agent for ARDS.
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http://dx.doi.org/10.1007/s10753-019-01020-2DOI Listing
October 2019

Propolis and Its Combination with Boric Acid Protect Against Ischemia/Reperfusion-Induced Acute Kidney Injury by Inhibiting Oxidative Stress, Inflammation, DNA Damage, and Apoptosis in Rats.

Biol Trace Elem Res 2019 Dec 19;192(2):214-221. Epub 2019 Feb 19.

Department of Chemistry, Faculty of Science, Dokuz Eylül University, Izmir, Turkey.

Ischemia reperfusion (I/R) injury which causes kidney dysfunction is one of the most studied diseases directly linked to oxidative stress. In this regard, it is important to protect cells against damage by inducing antioxidant response. Herein, we aimed to evaluate the therapeutic roles and possible mechanisms of propolis and boric acid in kidney I/R injury based on relevant basic research and clinical studies. Sprague-Dawley rats were subjected to 50 min of ischemia followed by 3 h of reperfusion. Animals were randomly divided into a control group (the abdominal wall was just opened and closed), an I/R injury group, the propolis intervention group (200 mg/kg, intragastric administration, 1 h before ischemia), boric acid intervention group (14 mg/kg, intragastric administration 1 h before ischemia), and the propolis + boric acid intervention group (intragastric administration 1 h before ischemia). Kidney function, the antioxidant defensive system, and renal damage were assessed. In addition, the oxidative stress and inflammatory status were estimated in renal tissue. Furthermore, DNA damageand apoptosis were detected by immunohistochemistry. When compared with I/R group, propolis alone and especially propolis + boric acid groups significantly improved functional parameters. While the antioxidant response was increased, renal injury size and apoptosis were significantly decreased in both groups. Also, the MDA and TNF-α levels besides the 8-OHdG formation were downregulated. According to these outcomes, it can be said that especially propolis together with boric acid ameliorates kidney injury caused by I/R through acting as an antioxidant, anti-inflammatory, and antiapoptotic agent. In conclusion, propolis alone and its combination with boric acid could be developed as therapeutic agents against serious renal I/R injuries.
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http://dx.doi.org/10.1007/s12011-019-1649-2DOI Listing
December 2019

Anti-inflammatory and antioxidant properties of jervine, a sterodial alkaloid from rhizomes of Veratrum album.

Phytomedicine 2019 Mar 11;55:191-199. Epub 2018 Aug 11.

Department of Chemistry, Faculty of Science and Letters, Kilis 7 Aralik University, 79000 Kilis, Turkey. Electronic address:

Background: Veratrum, hellebore is an important plant species of the Liliaceae family and jervine is the characteristic steroidal alkaloid constituent of Veratrum album.

Purpose: In the current study, anti-inflammatory and antioxidant effects of jervine isolated from NHOH-benzene extract of V. album rhizomes were investigated on CAR induced paw edema in rats.

Methods/study Design: In inflammatory study, 50, 100, 200 and 400  mg/kg doses of jervine, 25  mg/kg doses of DIC and IND were orally administered, and the volume of the foots were measured up to their knee arthrosis by plethismometer. After one hour of the oral administration of the all treatments, 0.1 ml of CAR solution (1%) was injected into the foot of the all rat groups and the volume of the foots were measured during 5 h after CAR injection. GPx, SOD, GR, MPO, CAT enzymes activities and GSH, LPO levels of the supernatants of paw homogenates and inflammation biomarkers such as TNF-α and IL-1β in the rats serums were also estimated.

Results: According to the present results, jervine exerted 50.4-73.5% anti-inflammatory effects in carrageenan induced paw edema. Inflammation biomarkers such as TNF-α, IL-1β and MPO that increased by CAR injection were suppressed by the administrations of all doses of jervine, IND and DIC. In all paw tissues, LPO levels as indicator of oxidative tissue damage were found to be high in CAR-treated group and it was found to be decreased in all doses of jervine.

Conclusion: Jervine, DIC and IND reduced the negative effects of CAR due to increasing effects on the SOD, CAT, GSH, GPx and GR antioxidants.
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http://dx.doi.org/10.1016/j.phymed.2018.06.035DOI Listing
March 2019

The protective effect of propolis on rat ovary against ischemia-reperfusion injury: Immunohistochemical, biochemical and histopathological evaluations.

Biomed Pharmacother 2019 Mar 3;111:631-637. Epub 2019 Jan 3.

Department of Biology, Faculty of Science, Ataturk University, Erzurum, Turkey.

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http://dx.doi.org/10.1016/j.biopha.2018.12.113DOI Listing
March 2019

Hepatoprotective Role of Thymol in Drug-Induced Gastric Ulcer Model.

Ann Hepatol 2018 Oct;17(6):980-991

Department of Biology, Faculty of Science, Ataturk University, Erzurum, TURKEY.

Introduction And Aim: Indo is widely one of the non-steroidal anti-inflammatory drugs and one of the common toxic effects of this drug is hepatic failure. Thymol is a monoterpene phenol with many different pharmacological activities. However, up to now its hepatoprotective effects on Indo-induced gastric ulcer model in rats have not been explored yet.

Material And Methods: Thirty five Sprague-Dawley rats were divided into seven groups: control, ulcer control (30 mg/kg Indo), Indo + reference standard (50 mg/kg Rantidine), Indo + Thymol (75, 100, 250 and 500 mg/kg) groups. 10 minutes after the induction of ulcer with Indo; Thymol was orally administered to the rats. Liver function enzymes (AST, ALT and LDH) were measured from serum samples. TOS/TAC, TNF-α and PGE2 levels, eNOS and Caspase-3 activity were assessed from tissue homogenate samples. In addition, histopathologic analysis on liver sections was performed.

Results: Indo significantly increased the levels of hepatic enzymes, TNF-α and eNOS, and caspase-3 activation, while decreased PGE2 levels. Furthermore, it induced oxidative stress as evidenced by elevated TOS and decreased TAC levels. However, Thymol treatment induced a significant improvement in these parameters, especially in 250 mg/kg dose. On the other hand, treatment with Thymol 500 mg/kg dramatically affected the parameters much worse than the Indo treated group.

Conclusion: The findings of the current study demonstrated that Thymol administration significantly ameliorated liver injury due to Indo toxicity. This effect of Thymol (250 mg/kg) may be mediated by its anti-oxidative or anti-inflammatory effect, and up-regulation the synthesis of PGE2.
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http://dx.doi.org/10.5604/01.3001.0012.7198DOI Listing
October 2018

Gastroprotective effects of oleuropein and thymol on indomethacin-induced gastric ulcer in Sprague-Dawley rats.

Drug Chem Toxicol 2020 Sep 14;43(5):441-453. Epub 2018 Nov 14.

Department of Biology, Faculty of Science, Ataturk University, Erzurum, Turkey.

Ethnopharmacological studies demonstrated that thymol (Thym) and oleuropein (Ole) have therapeutic potential for gastric ulcers. The molecular mechanism underlying the gastroprotective effects of these compounds have not been elucidated yet especially for their individual and combination use at high dose. Therefore, this study was conducted to explore their gastroprotective mechanisms on indomethacin (Indo)-induced gastric ulcer model. Ole (50,100, 250, and 500 mg/kg) and Thym (50,100, 200, and 500 mg/kg) were orally administered to the rats 10 min before the induction of ulcer with Indo. The combination of 500 mg/kg doses of Ole and Thym were applied. The gastric mucosa was evaluated histopathologically. Moreover, TAC/TOS, tumor necrosis factor-alpha (TNF-α), prostaglandin E (PGE), endothelial nitric oxide synthase (eNOS), and caspase-3 levels were assessed by ELISA and the caspase-3 and TNF-α expressions were quantified by qRT-PCR. Indo-induced histopathological changes while Ole and Thym pretreatment prevented these effects. Unlike the 500 mg/kg dose of Ole treatment, the 500 mg/kg dose of Thym administration enhanced these damages. The decreased TAC, PGE levels and increased TOS, eNOS, TNF-α, caspase-3 levels were obtained in Indo group. However, these changes were reversed by Ole and Thym groups except the 500 mg/kg dose of Thym and the combination treatment groups. Similar trends were observed in the caspase-3 and TNF-α expression levels. These results demonstrated that enhanced inflammation, oxidant/antioxidant imbalance, and apoptotic activities were occurred in Indo, 500 mg/kg dose of Thym and the combination treatment groups while not in the other groups. The findings demonstrated the gastroprotective ability of Ole and low doses of Thym in gastric ulcer models.
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http://dx.doi.org/10.1080/01480545.2018.1530261DOI Listing
September 2020

Effect of melatonin on antioxidant capacity, ınflammation and apoptotic cell death in lung tissue of diabetic rats.

Acta Cir Bras 2018 Apr;33(4):375-385

Full Professor, Department of Anesthesiology and Reanimation, Faculty of Medicine, Erzincan University, Turkey. Manuscript writing.

Purpose: To investigate the effects of melatonin on antioxidant capacity, inflammation and apoptotic cell death (through expression of cleaved-caspase 3) in lung tissue samples of diabetic rats.

Methods: Thirty male Sprague-Dawley rats were randomly divided into three groups. Group 1 (control group) was made up of healthy rats. Group 2 (diabetes group) received streptozotocin at a dose of 50 mg/kg/day for 5 days.Group 3 (diabetes plus melatonin group) received streptozotocin at a dose of 50 mg/kg/day for 5 days and then they received melatonin at a dose of 20 mg/kg/day between 28thand 35thdays of the study.

Results: Tissue MDA and MPO levels were found to be significantly higher in diabetes group compared to control group (p<0.05) whilst administration of melatonin was found to significantly lower this increase down to normal levels (p<0.05). Bronchus associated lymphoid tissue (BALT) was more severe in diabetics whereas administration of melatonin alleviated this hyperplasia. Cleaved caspase 3 activity was severe in hyperplastic BALT in diabetic rats however in lowered down to moderate level when melatonin was administered.

Conclusion: The melatonin caused an increase in antioxidant capacity and decreased the expression of cleaved-caspase 3.
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http://dx.doi.org/10.1590/s0102-865020180040000009DOI Listing
April 2018

A novel therapeutics agent: antioxidant effects of hydroxylfasudil on rat kidney and liver tissues in a protamine sulphate-induced cystitis rat model; preliminary results.

Artif Cells Nanomed Biotechnol 2018 9;46(sup2):9-14. Epub 2018 Mar 9.

i Department of Biochemistry , Erzincan University , Erzincan , Turkey.

Cystitis is defined as an inflammation of the bladder caused by a bacterial infection, and it can be dangerous and painful when it spreads through the internal organs. In this study, antioxidant effects of hydroxylfasudil (HF) at the enzymatic and molecular level on kidney and liver tissues in cystitis rat model, which is caused by inflammation of the rat bladder with a protamine sulphate (PS), was examined. Quantitative changes of reduced glutathione (GSH) and lipid peroxidation (LPO) levels, which are a marker for oxidative stress, were determined in rat kidney and liver tissues for each groups. And then molecular and biochemical impact of HF treatment on antioxidant enzymes including superoxide dismutase (SOD) and catalase (CAT) in cystitis model were studied. The results suggest that HF could be beneficial to the renal and hepatic antioxidant system. Thus, HF might be used as a novel therapeutics agent to eliminate interstitial cystitis.
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http://dx.doi.org/10.1080/21691401.2018.1449120DOI Listing
June 2019

Impact of high-dose oleuropein on cisplatin-induced oxidative stress, genotoxicity and pathological changes in rat stomach and lung.

J Asian Nat Prod Res 2017 Dec 21;19(12):1214-1231. Epub 2017 Apr 21.

d Faculty of Veterinary, Department of Pathology , Ataturk University , Erzurum 25040 , Turkey.

The current systemic treatments of the various solid tumors involve Cisplatin (CIS)-based chemotherapy. Due to its cytotoxicity, this approach is limited. Moreover, the safety of CIS is only discussed especially in breast and stomach cancers. Therefore, we, for the first time, explored the restorative efficacy of oleuropein (OLE), in stomach and lung injuries induced by CIS. Sprague-Dawley rats were divided into eight groups: control CIS, OLE and CIS + OLE. Single dose of (7 mg/kg) CIS was administered intraperitoneally to CIS and CIS + OLE groups. After 24 h, 50, 100 and 200 mg/kg OLE was given for three consecutive days to OLE and CIS + OLE groups. The 8-OH-dG, total oxidative/antioxidant status (TOS/TAS) and malondialdehyde (MDA) levels were evaluated and histopathological analyses were performed on the studied tissues. The results indicated that CIS significantly increased 8-OH-dG, MDA and TOS levels and caused severe tissue damages. However, high dose of OLE induced a significant decrease in the 8-OH-dG, MDA levels, an increase in TAS levels and it restores CIS-induced tissue damages. We hope that the results of this study will provide an impetus for future studies on novel therapeutic strategies including the protective use of oleuropein in gastric and lung cancers due to chemotherapy.
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http://dx.doi.org/10.1080/10286020.2017.1317751DOI Listing
December 2017

Natural product inhibitors of carbonic anhydrase I and II isoenzymes: osajin and pomiferin.

Arch Physiol Biochem 2017 Oct 24;123(4):219-224. Epub 2017 Mar 24.

b Faculty of Veterinary, Department of Biochemistry , Ataturk University , Erzurum , Turkey.

The aim of this study is to purify carbonic anhydrase I and II isoenzymes from human erythrocyte, isolate two natural products osajin (OSJ) and pomiferin (PMF) from Maclura pomifera fruits, and evaluate the in vitro effect of these natural metabolites on these isoenzymes. These natural products may be used as starting points for drug discovery (like drugs used in several therapeutic applications, including antiglaucoma activity). For the purification procedure, the Sepharose-4B-l-tyrosine-sulphonamide affinity chromatography was used. Column chromatography and thin layer chromatography methods were used for isolation of OSJ and PMF from M. pomifera fruits and their chemical structures were elucidated by IR, 1D, and 2D NMR methods. We compared inhibitory effects of these natural products with inhibitory effects of phenolic compounds and found that these products demonstrated average inhibition effects. We thought that this study will give inspiration to scientists interested in this issue.
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http://dx.doi.org/10.1080/13813455.2017.1303742DOI Listing
October 2017

Evaluation of 8-hydroxy-2-deoxyguanosine and NFkB activation, oxidative stress response, acetylcholinesterase activity, and histopathological changes in rainbow trout brain exposed to linuron.

Environ Toxicol Pharmacol 2017 Jan 13;49:14-20. Epub 2016 Nov 13.

Department of Aquaculture, Faculty of Fisheries, Ataturk University, TR-25030 Erzurum, Turkey.

Linuron is a widely used herbicide to control grasses and annual broad leaf weeds. It is known that linuron has toxic effects on different organisms. However, the toxic effects of linuron on aquatic organisms, especially fish, is completely unknown. Thus, we aimed to investigate changes in 8-hydroxy-2-deoxyguanosine (8-OHdG) and nuclear factor kappa B (NFkB) activity, histopathological changes, antioxidant responses and acetylcholinesterase (AChE) activity in rainbow trout brain after exposure to linuron. Fish were exposed to 30μg/L, 120μg/L and 240μg/L concentrations of linuron for twenty-one days. Brain tissues were taken from fish for 8-OHdG and NFkB activity, histopathological examination and determination of superoxide dismutase (SOD), catalase (CAT) enzyme activity, lipid peroxidation (LPO), and reduced glutathione (GSH) levels. Our data indicated that high linuron concentrations caused a decrease in GSH levels, SOD and CAT activities in brain tissues (p<0.05). LPO levels were significantly increased by 240μg/L linuron. All concentrations caused a significant inhibition in brain AChE enzyme activity (p<0.05). Immunopositivity was detected for 8-OHdG and NFkB, and linuron exposure caused histopathological damage to the brain tissues. The results of this study can provide useful information for understanding of linuron-induced toxicity.
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http://dx.doi.org/10.1016/j.etap.2016.11.009DOI Listing
January 2017

Physiological and biochemical effects of nickel on rainbow trout (Oncorhynchus mykiss) tissues: Assessment of nuclear factor kappa B activation, oxidative stress and histopathological changes.

Chemosphere 2017 Jan 2;166:445-452. Epub 2016 Oct 2.

Department of Biochemistry, Faculty of Veterinary, Ataturk University, TR-25240, Erzurum, Turkey.

We investigated changes in nuclear factor kappa B (NFkB) activity, antioxidant responses and histopathological effects in the liver, gill and kidney tissues of rainbow trout exposed to nickel chloride (Ni). Two different concentrations (1 mg/L and 2 mg/L) were administrated to fish for 21 days. Tissues were taken from all fish for NFkB activity, histopathological examination and determination of superoxide dismutase (SOD), catalase (CAT) enzyme activity and of lipid peroxidation (LPO), and glutathione (GSH) levels. The findings of this study indicated that Ni exposure led to a significant increase in LPO indicating peroxidative damage and antioxidant enzymes SOD and CAT activity in tissues (p < 0.05), but 2 mg/Ni concentration caused a significant decrease in CAT activity in kidney tissues (p < 0.05). One of mechanism in the antioxidant defense system seems to be GSH, which increased in gill and kidney tissues of fish exposed to Ni (p < 0.05). NFkB immunopositivity was detected in all tissues. Ni exposure caused lamellar thickening, cellular infiltration in gill tissues, hydropic degeneration of hepatocytes in liver tissues, hyalinous accumulation within the glomeruli and tubular degeneration in kidney tissues. Our results suggested that Ni toxicity may disturb the biochemical and physiological functions of fish by causing changes in NFkB activity and oxidative and histopathological damage in the tissues of rainbow trout. This study can provide useful information for understanding of Ni-induced toxicity.
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http://dx.doi.org/10.1016/j.chemosphere.2016.09.106DOI Listing
January 2017

Pernicious effects of long-term, continuous 900-MHz electromagnetic field throughout adolescence on hippocampus morphology, biochemistry and pyramidal neuron numbers in 60-day-old Sprague Dawley male rats.

J Chem Neuroanat 2016 11 16;77:169-175. Epub 2016 Jul 16.

Department of Histology and Embryology, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkey. Electronic address:

The central nervous system (CNS) begins developing in the intrauterine period, a process that continues until adulthood. Contact with chemical substances, drugs or environmental agents such as electromagnetic field (EMF) during adolescence therefore has the potential to disturb the development of the morphological architecture of components of the CNS (such as the hippocampus). The hippocampus is essential to such diverse functions as memory acquisition and integration and spatial maneuvering. EMF can result in severe damage to both the morphology of the hippocampus and its principal functions during adolescence. Although children and adolescents undergo greater exposure to EMF than adults, the information currently available regarding the effects of exposure to EMF during this period is as yet insufficient. This study investigated the 60-day-old male rat hippocampus following exposure to 900 megahertz (MHz) EMF throughout the adolescent period using stereological, histopathological and biochemical analysis techniques. Eighteen male Sprague Dawley rats aged 21days were assigned into control, sham and EMF groups on a random basis. No procedure was performed on the control group rats. The EMF group (EMFGr) was exposed to a 900-MHz EMF for 1h daily from beginning to end of adolescence. The sham group rats were held in the EMF cage but were not exposed to EMF. All rats were sacrificed at 60days of age. Their brains were extracted and halved. The left hemispheres were set aside for biochemical analyses and the right hemispheres were subjected to stereological and histopathological evaluation. Histopathological examination revealed increased numbers of pyknotic neurons with black or dark blue cytoplasm on EMFGr slides stained with cresyl violet. Stereological analyses revealed fewer pyramidal neurons in EMFGr than in the other two groups. Biochemical analyses showed an increase in malondialdehyde and glutathione levels, but a decrease in catalase levels in EMFGr. Our results indicate that oxidative stress-related morphological damage and pyramidal neuron loss may be observed in the rat hippocampus following exposure to 900-MHz EMF throughout the adolescent period.
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http://dx.doi.org/10.1016/j.jchemneu.2016.07.004DOI Listing
November 2016

The protective effects of epigallocatechin gallate on lipopolysa ccharide-induced hepatotoxicity: an in vitro study on Hep3B cells.

Iran J Basic Med Sci 2016 May;19(5):483-9

Department of Pharmacology and Toxicology, Veterinary Faculty, Ataturk University, Erzurum, Turkey.

Objectives: In the present study, our aim was to investigate the possible protective effects of epigallocatechin gallate (EGCG) on lipopolysaccharide (LPS)-induced hepatotoxicity by using Hep3B human hepatoma cells. Specifically, the study examines the role of some proinflammatory markers and oxidative damage as possible mechanisms of LPS-associated cytotoxicity. Consequently, the hepatocellular carcinoma cell line Hep3B was chosen as a model for investigation of LPS toxicity and the effect of EGCG on LPS-exposed cells.

Materials And Methods: The Hep3B human hepatoma cells were used for this study. The cytotoxic effects of chemicals (EGCG and LPS), AST and ALT levels, SOD and CAT activities, GSH-Px level and TNF-alpha and IL-6 levels were detected by using different biochemical and molecular methods. LPS and EGCG were applied to cells at various times and doses.

Results: The highest treatment dose of EGCG (400 µM) led to a dramatic decrease in SOD level and increase in CAT and GSH levels. Additionally, the highest dose of EGCG also led to a dramatic increase in TNF-alpha and IL-6 levels. On the other hand, effective doses of EGCG (200 and 100 µM) normalized all related parameters levels.

Conclusion: LPS caused hepatotoxicity, but interestingly, a high dose of EGCG was found to be a cytotoxic agent in this study. However, other two doses of EGCG led to a decrease in both inflammatory cytokine levels and antioxidant enzyme levels. Further studies should examine the effect of EGCG on secondary cellular signaling pathways.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4923468PMC
May 2016

Anti-oxidant and anti-inflammatory effects of apigenin in a rat model of sepsis: an immunological, biochemical, and histopathological study.

Immunopharmacol Immunotoxicol 2016 Jun;38(3):228-37

f Department of Histology and Embryology, Faculty of Medicine , Kafkas University , Kars , Turkey.

Objective: We hypothesize that apigenin may inhibit some cellular process of sepsis-induced spleen injury and simultaneously improve inflammation and oxidative stress. Therefore, the aim of this study was to investigate the potential protective effects of apigenin in a polymicrobial sepsis rat model of by cecal ligation and puncture.

Materials And Methods: 64 female Wistar albino rats were divided into 8 groups. The pro-inflammatory (tumor necrosis factor-alpha, interleukin-6, and interleukin-1-beta) and anti-inflammatory (tumor growth factor-beta and interleukin-10) cytokine levels were measured by enzyme-linked immunosorbent assay. CD3, CD68, and nuclear factor kappa B (NF-κB) positivity rates were detected by immunohistochemical methods. Oxidative stress parameters were measured by tissue biochemistry.

Results: Sepsis caused a significant increase in TNF-alpha, IL-1-beta, IL-6, and TGF-beta levels whereas it reduced IL-10 level. Additionally, it led to an increase in CD3, CD68, and NF-κB positivity rates as well as oxidative stress parameters levels. However, apigenin inhibited the inflammation process, increased the IL-10 level and normalized the oxidative stress parameters.

Discussion And Conclusion: Pretreatment with apigenin results in a significant reduction in the amount of inflammatory cells. The beneficial effect of apigenin on spleen injury also involved inhibition of NF-κB pathway, suppression of proinflammatory cytokines, and induction of anti-inflammatory cytokine production. Additionally, it led to a decrease in oxidative stress in spleen tissue. Taking everything into account, apigenin may be an alternative therapeutic option for prevention of sepsis-induced organ.
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http://dx.doi.org/10.3109/08923973.2016.1173058DOI Listing
June 2016

Melatonin Attenuates Contrast-Induced Nephropathy in Diabetic Rats: The Role of Interleukin-33 and Oxidative Stress.

Mediators Inflamm 2016 18;2016:9050828. Epub 2016 Feb 18.

Department of Cardiology, Faculty of Medicine, Erzincan University, Erzincan, Turkey.

Background: Inflammation and oxidative stress (OxS) contribute to the pathogenesis of diabetic kidney disease (DKD) and contrast-induced nephropathy (CIN). Patients with DKD were found to be more prone to CIN. Interleukin-33 (IL-33) is a proinflammatory cytokine, but its role in DKD and CIN is unknown.

Methods: Thirty male Sprague-Dawley rats were enrolled. The first group was comprised of healthy rats (HRs), whereas the other four groups were made up of diabetic rats (DRs), diabetic rats with contrast-induced nephropathy (CIN + DRs), melatonin-treated diabetic rats (MTDRs), and melatonin-treated CIN + DRs (MTCIN + DRs). All groups except the HRs received 50 mg/kg/day streptozotocin (STZ). CIN + DRs were constituted by administrating 1.5 mg/kg of intravenous radiocontrast dye on the 35th day. MTDRs and MTCIN + DRs were given 20 mg/kg/day of intraperitoneal injection of melatonin (MT) from the 28th day for the constitutive seven days.

Results: We observed increased IL-33 in the kidney tissue following induction of CIN in DRs. To determine whether MT is effective in preventing CIN, we administered MT in CIN + DRs and demonstrated that kidney tissue levels of OxS markers, inflammatory cytokines, and IL-33 were significantly diminished in MTCIN + DRs compared with other groups without MT treatment (p < 0.05).

Conclusion: Inhibition of IL-33 with MT provides therapeutic potential in DKD with CIN.
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http://dx.doi.org/10.1155/2016/9050828DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4775802PMC
December 2016

Morphological and antioxidant impairments in the spinal cord of male offspring rats following exposure to a continuous 900MHz electromagnetic field during early and mid-adolescence.

J Chem Neuroanat 2016 09 17;75(Pt B):99-104. Epub 2015 Dec 17.

Department of Histology and Embryology, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkey. Electronic address:

The effects of devices emitting electromagnetic field (EMF) on human health have become the subject of intense research among scientists due to the rapid increase in their use. Children and adolescents are particularly attracted to the use of devices emitting EMF, such as mobile phones. The aim of this study was therefore to investigate changes in the spinal cords of male rat pups exposed to the effect of 900MHz EMF. The study began with 24 Sprague-Dawley male rats aged 3 weeks. Three groups containing equal numbers of rats were established-control group (CG), sham group (SG) and EMF group (EMFG). EMFG rats were placed inside an EMF cage every day between postnatal days (PD) 21 and 46 and exposed to the effect of 900MHz EMF for 1h. SG rats were kept in the EMF cage for 1h without being exposed to the effect of EMF. At the end of the study, the spinal cords in the upper thoracic region of all rats were removed. Tissues were collected for biochemistry, light microscopy (LM) and transmission electron microscopic (TEM) examination. Biochemistry results revealed significantly increased malondialdehyde and glutathione levels in EMFG compared to CG and SG, while SG and EMFG catalase and superoxide dismutase levels were significantly higher than those in CG. In EMFG, LM revealed atrophy in the spinal cord, vacuolization, myelin thickening and irregularities in the perikarya. TEM revealed marked loss of myelin sheath integrity and invagination into the axon and broad vacuoles in axoplasm. The study results show that biochemical alterations and pathological changes may occur in the spinal cords of male rats following exposure to 900MHz EMF for 1h a day on PD 21-46.
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http://dx.doi.org/10.1016/j.jchemneu.2015.11.006DOI Listing
September 2016

The effects of prenatal long-duration exposure to 900-MHz electromagnetic field on the 21-day-old newborn male rat liver.

Turk J Med Sci 2015 ;45(2):291-7

Background/aim: To determine what effect a 900-MHz electromagnetic field (EMF) applied in the prenatal period would have on the liver in the postnatal period.

Materials And Methods: At the start of the study, adult pregnant rats were divided into two groups, control and experimental. The experimental group was exposed to a 900-MHz EMF for 1 h daily during days 13-21 of pregnancy. After birth, no procedure was performed on either mothers or pups. Male rat pups (n = 6) from the control group mothers (CGMR) and male rat pups (n = 6) from the experimental group mothers (EGMR) were sacrificed on postnatal day 21.

Results: Biochemical analyses showed that malondialdehyde and superoxide dismutase values increased and glutathione levels decreased in the EGMR pups. Marked hydropic degeneration in the parenchyma, particularly in pericentral regions, was observed in light microscopic examination of EGMR sections stained with hematoxylin and eosin. Examinations under transmission electron microscope revealed vacuolization in the mitochondria, expansion in the endoplasmic reticulum, and necrotic hepatocytes.

Conclusion: The study results show that a 900-MHz EMF applied in the prenatal period caused oxidative stress and pathological alterations in the liver in the postnatal period.
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http://dx.doi.org/10.3906/sag-1404-168DOI Listing
July 2015

The effect of silymarin on hepatic regeneration after partial hepatectomy: is silymarin effective in hepatic regeneration?

Int J Clin Exp Med 2015 15;8(2):2578-85. Epub 2015 Feb 15.

Medikal Park Hastanesi, Genel Cerrahi Klinigi Elazig, Turkiye.

Aim: Silymarin from Silybum marianum was found to reduce liver injury. The aim of the present study was to investigate the effects of silymarin on hepatic regeneration in partially hepatectomized rats.

Methods: Thirty Wistar-Albino rats were divided into 3 groups of 10 animals as sham, control and experimental groups. In the sham group (n=10) abdominal incision was closed after laparotomy. In the control group (n=10), the rats underwent 70% hepatectomy after laparotomy. In the experimental group (n=10) after partial 70% hepatectomy, silymarin (200 mg/kg/d) were given to rats for 10 days. Rats in three groups were sacrificed on 10 days. Aspartate (AST) and alanine transaminase (ALT), gamma glutamyl transferase (GGT), ALP, LDH and total bilirubin levels were measured using intracardiac blood samples. Tissue malondialdehyde (MDA) and tissue glutathion (GSH) and Superoxide dismutase (SOD) levels were measured. To reveal the increase in the mass of the remnant liver tissue in the control and experimental groups relative weight of the liver was calculated. Histopathological analysis of the liver was performed using a semi-quantitative scoring system.

Results: A statistically significant difference among three groups was not shown for AST and ALT levels. A statistically significant difference was found between the groups as for total bilirubin and gamma glutamyl transferase levels. Increases in relative liver weights were seen with time in Groups 2 and 3. A statistically significant difference was not found for tissue malondialdehyde, Glutathion and Superoxide dismutase levels between hepatectomy and hepatectomy + silymarin groups. On liver tissue sections of the rats in the hepatectomy + silymarin group, increased regeneration and lipid peroxidation were observed accompanied by decreased antioxidant response.

Conclusion: It has been observed that silymarin with many established functions such as antiproliferative, anti-inflammatory and energy antioxidant effects, does not contributed to proliferative regeneration of the liver-which has very important metabolic functions -after partial hepatectomy; instead it will decrease serum levels of transaminases.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4402851PMC
May 2015

Neurotoxic effects of nickel chloride in the rainbow trout brain: Assessment of c-Fos activity, antioxidant responses, acetylcholinesterase activity, and histopathological changes.

Fish Physiol Biochem 2015 Jun 10;41(3):625-34. Epub 2015 Feb 10.

Department of Basic Sciences, Faculty of Fisheries, Ataturk University, 25240, Erzurum, Turkey,

The aim of this study was to determine the biochemical, immunohistochemical, and histopathological effects of nickel chloride (Ni) in the rainbow trout brain. Fish were exposed to Ni concentrations (1 mg/L and 2 mg/L) for 21 days. At the end of the experimental period, brain tissues were taken from all fish for c-Fos activity and histopathological examination and determination of acetylcholinesterase (AChE), superoxide dismutase (SOD), catalase (CAT) enzyme activities, lipid peroxidation (LPO), and glutathione (GSH) levels. Our results showed that Ni treatment caused a significant increase in the brain SOD activity and in LPO and GSH levels (p < 0.05), but it significantly decreased AChE and CAT enzyme activities (p < 0.05). Strong induction in c-Fos was observed in some cerebral and cerebellar regions of fish exposed to Ni concentrations when compared with the control group. However, c-Fos activity was decreased in necrotic Purkinje cells. Brain tissues were characterized by demyelination and necrotic changes. These results suggested that Ni treatment causes oxidative stress, changes in c-Fos activity, and histopathological damage in the fish brain.
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http://dx.doi.org/10.1007/s10695-015-0033-1DOI Listing
June 2015

Stimulation of gene expression and activity of antioxidant related enzyme in Sprague Dawley rat kidney induced by long-term iron toxicity.

Comp Biochem Physiol C Toxicol Pharmacol 2014 Nov 16;166:44-50. Epub 2014 Jul 16.

Atatürk University, Science Faculty, Department of Molecular Biology and Genetics, 25240 Erzurum, Turkey.

The trace elements such as iron are vital for various enzyme activities and for other cellular proteins, but iron toxicity causes the production of reactive oxygen species (ROS) that causes alterations in morphology and function of the nephron. The present study was designed to determine the effect of long-term iron overload on the renal antioxidant system and to determine any possible correlation between enzymatic and molecular levels. Our data showed that reduced glutathione (GSH) levels, which is a marker for oxidative stress, strikingly decreased with a long-term iron overload in rat kidney. While renal mRNA levels of glucose 6-phosphate dehydrogenase (G6pd), 6-phosphogluconate dehydrogenase (6pgd) and glutathione peroxidase (Gpx) were significantly affected in the presence of ferric iron, no changes were seen for glutathione reductase (Gsr) and glutathione S-transferases (Gst). While the iron affected the enzymatic activity of G6PD, GSR, GST, and GPX, it had no significant effect on 6PGD activity in the rat kidney. In conclusion, we reported here that the gene expression of G6pd, 6pgd, Gsr, Gpx, and Gst did not correlate to enzyme activity, and the actual effect of long-term iron overload on renal antioxidant system is observed at protein level. Furthermore, the influence of iron on the renal antioxidant system is different from its effect on the hepatic antioxidant system.
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http://dx.doi.org/10.1016/j.cbpc.2014.07.002DOI Listing
November 2014