Publications by authors named "Mahsa Hamzeh"

9 Publications

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Effects of TiO2 nanoparticles on ROS production and growth inhibition using freshwater green algae pre-exposed to UV irradiation.

Environ Toxicol Pharmacol 2015 May 1;39(3):1074-80. Epub 2015 Apr 1.

National Research Council of Canada, 6100 Royalmount Avenue, Montreal, Quebec H4P 2R2, Canada; Department of Natural Resource Sciences, McGill University, 21111 Lakeshore Road, Ste-Anne-de-Bellevue, Quebec H9X 3V9, Canada. Electronic address:

This study investigated the possibility that titanium dioxide nanoparticles (nano-TiO2) toxicity in Pseudokirchneriella subcapitata involves reactive oxygen species (ROS) production, using the dichlorodihydrofluorescein (DCF) assay. Algae were exposed to nano-TiO2 under laboratory fluorescent lamps supplemented with UV irradiation for 3h, with or without a UV filter. Results showed that nano-TiO2 increased ROS production in UV-exposed cells, with or without a UV filter (LOEC values were 250 and 10mg/L, respectively). Sublethal effects of nano-TiO2 on UV pre-exposed algae were also examined. Toxicity studies indicated that exposure to nano-TiO2 agglomerates decreased algal growth following 3h pre-exposure to UV, with or without a UV filter (EC50s were 8.7 and 6.3mg/L, respectively). The present study suggests that the growth inhibitory effects of nano-TiO2 in algae occurred at concentrations lower than those that can elevate DCF fluorescence, and that ROS generation is not directly involved with the sublethal effects of nano-TiO2 in algae.
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http://dx.doi.org/10.1016/j.etap.2015.03.015DOI Listing
May 2015

Monitoring of potential cytotoxic and inhibitory effects of titanium dioxide using on-line and non-invasive cell-based impedance spectroscopy.

Anal Chim Acta 2013 May 26;777:78-85. Epub 2013 Mar 26.

National Research Council Canada, 6100 Royalmount Avenue, Montreal, Quebec H4P 2R2, Canada.

Titanium dioxide (TiO2) nanoparticles (NPs) with different sizes and structures were probed for plausible cytotoxicity using electric cell-substrate impedance sensing (ECIS), a non-invasive and on-line procedure for continuous monitoring of cytotoxicity. For insect cells (Spodoptera frugiperda Sf9), the ECIS50 values, i.e., the concentration required to achieve 50% inhibition of the response, differed depending on the size and shape of the TiO2 nanostructure. The lowest ECIS50 value (158 ppm) was observed for the needle shaped rutile TiO2 (10 nm×40 nm, 15.5 nm nominal particle size), followed by 211 ppm for P-25 (34.1 nm, 80% anatase and 20% rutile), 302 ppm for MTI5 (5.9 nm, 99% anatase) and 417 ppm for Hombitan LW-S bulk TiO2 (169.5 nm, 99% anatase). Exposure of TiO2 NPs to UV light at 254 nm or 365 nm exhibited no significant effect on the ECIS50 value due to the aggregation of TiO2 NPs with diminishing photocatalytic activities. Chinese hamster lung fibroblast V79 cells, exhibited no significant cytotoxicity/inhibition up to 400 ppm with P25, MTI5 and bulk TiO2. However, a noticeable inhibitory effect was observed (ECIS50 value of 251 ppm) with rutile TiO2 as cell spreading on the electrode surface was prevented.
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http://dx.doi.org/10.1016/j.aca.2013.03.044DOI Listing
May 2013

In vitro cytotoxicity and genotoxicity studies of titanium dioxide (TiO2) nanoparticles in Chinese hamster lung fibroblast cells.

Toxicol In Vitro 2013 Mar 28;27(2):864-73. Epub 2012 Dec 28.

National Research Council Canada, 6100 Royalmount Ave., Montréal, QC H4P 2R2, Canada.

There are increasing safety concerns about the development and abundant use of nanoparticles. The unique physical and chemical characteristics of titanium dioxide (TiO2) nanoparticles result in different chemical and biological activities compared to their larger micron-sized counterparts, and can subsequently play an important role in influencing toxicity. Therefore, our objective was to investigate the cytotoxicity and genotoxicity of commercially available TiO2 nanoparticles with respect to their selected physicochemical properties, as well as the role of surface coating of these nanoparticles. While all types of tested TiO2 samples decrease cell viability in a mass-based concentration- and size-dependent manner, the polyacrylate-coated nano-TiO2 product was only cytotoxic at higher concentrations. A similar pattern of response was observed for induction of apoptosis/necrosis, and no DNA damage was detected in the polyacrylate-coated nano-TiO2 model. Given the increasing production of TiO2 nanoparticles, toxicological studies should take into account the physiochemical properties of these nanoparticles that may help researchers to develop new nanoparticles with minimum toxicity.
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http://dx.doi.org/10.1016/j.tiv.2012.12.018DOI Listing
March 2013

Androgen action in the epididymis.

J Androl 2011 Nov-Dec;32(6):592-9. Epub 2011 Jul 15.

Department of Pharmacology & Therapeutics, McGill University, 3655 Promenade Sir William Osler, Montreal, Quebec, Canada.

Androgens are responsible for maintaining epididymal structure and functions. However, little is known about how androgen action is mediated and the mechanisms underlying the restoration of the integrity of epididymal cells after androgen deprivation. We first provide an overview of what is known about androgen action in this tissue and then present data on the initial and sequential roles of androgens in altering cellular architecture and function in an androgen-deprived condition. Using morphometric analysis and the rat model, we identified changes in epithelial cell height and lumen diameter, as well as in the numbers of proliferating cells in different regions and at various time points after androgen withdrawal and replacement. The sequence of gene activation or suppression that occurred in the androgen-deprived tissue was examined upon the readministration of the 2 active metabolites of testosterone, dihydrotestosterone (DHT) and estradiol. Although few genes were regulated by estradiol, many were affected by DHT. Epidermal growth factor (EGF) and insulinlike growth factor-1 (IGF1) appear to play an important role in the early response pathway activated by DHT because of their function in the regulation of the expression of many other genes. The intracellular signaling pathway involved in mediating the action of androgen in restoring epididymal epithelial cell integrity was investigated using the PC-1 epididymal cell line. IGF1 and EGF receptors were found to be important mediators of androgen receptor-mediated activation of the MAPK/ERK pathways. Together, these studies provide a greater understanding of the mechanisms of androgen action in the epididymis.
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http://dx.doi.org/10.2164/jandrol.111.014266DOI Listing
February 2012

Androgens activate mitogen-activated protein kinase via epidermal growth factor receptor/insulin-like growth factor 1 receptor in the mouse PC-1 cell line.

J Endocrinol 2011 Apr 10;209(1):55-64. Epub 2011 Jan 10.

Department of Pharmacology and Therapeutics, McGill University, McIntyre Medical Sciences Building, 3655 Promenade Sir-William-Osler, Montréal, Québec, Canada.

Androgens are the primary regulators of epididymal structure and functions. In the classical view of androgen action, binding of androgen to the intracellular androgen receptor (AR) produces the receptor-steroid complex that has high affinity for DNA response elements and regulates the transcription of target genes. In this study, we demonstrate that in epididymal cells, 5α-dihydrotestosterone (DHT) can cause an alternative and rapid response that is independent of AR-DNA interactions and is mediated by activation of signaling pathways through the AR. We examined changes in AKT and extracellular signal-regulated protein kinases (ERK1/2) activation at early time points after DHT supplementation in the mouse proximal caput epididymis-1 cell line. DHT had no significant effect on AKT activation at any time point. However, DHT activated the ERK pathway as early as at 1 min, the pathway remained activated at 10 min, but activation was not sustained at later time points. Interestingly, ERK activation was blocked by hydroxyflutamide (HF), indicating that early ERK activation was an AR-mediated response. DHT phosphorylates steroid receptor co-activator (SRC) kinase, and this activation was required for the ERK response. EGFR and IGF1R were downstream of SRC, and these two receptors together contributed to enhance ERK and cAMP response element-binding protein (CREB) phosphorylation. We postulate that this rapid action of androgen may ultimately act to modulate the transcription of genes regulated by AR in the nucleus. These results support the hypothesis that DHT can activate a pathway involving the sequential activation of MEK, ERK1/2, and CREB through the EGFR/IGF1R in an epididymal cell line.
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http://dx.doi.org/10.1530/JOE-10-0223DOI Listing
April 2011

Identification of early response genes and pathway activated by androgens in the initial segment and caput regions of the regressed rat epididymis.

Endocrinology 2010 Sep 21;151(9):4504-14. Epub 2010 Jul 21.

Department of Pharmacology and Therapeutics, McGill University, 3655 Promenade Sir William Osler, Montreal, Quebec, Canada H3G1Y6.

To identify the initial response to androgens and estrogens in the orchidectomized, regressed epididymis, we determined the gene expression changes triggered by the administration of either of two metabolites of testosterone, 5alpha-dihydrotestosterone (DHT) or 17beta-estradiol (E2), in the regressed rat epididymis. Adult rats were orchidectomized and 8 d later implanted with either empty implants (control), DHT-filled-, or E2-filled-polydioxanone implants. Rats were euthanized 12 h, 1 d, and 7 d later, and RNA was extracted and probed on Rat230-2.0 Affymetrix arrays. Probe sets that respond to DHT or E2 were identified at early time points; although the expression of some was repressed, the expression of many others was either transiently or chronically elevated. Nerve growth factor receptor (Ngfr) and S100 calcium binding protein G (S100g) were two E2 up-regulated genes detected at 12 h. Among the genes that showed a dramatic early response to DHT were endothelin 1 (Edn1), bone morphogenetic protein 4 (Bmp4), and IGF binding protein 3 (Igfbp3), which were suppressed, and IGF-I (Igf1), which was induced. Genes that were up- or down-regulated by DHT were classified based on biological function. Using PathwayStudio 4.0, we identified genes that were linked and directly influenced either the expression or regulation of one another. Epidermal growth factor and IGF-I play an important role in the pathway due to their function in regulation and expression of many other genes. These results provide novel insights into the impact of androgen action on the expression of genes that are important for epididymal function.
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http://dx.doi.org/10.1210/en.2010-0023DOI Listing
September 2010

Effect of testosterone on epithelial cell proliferation in the regressed rat epididymis.

J Androl 2009 Mar-Apr;30(2):200-12. Epub 2008 Oct 16.

McIntyre Medical Sciences Building, 3655 Promenade Sir-William-Osler, Montréal, Québec, Canada.

It is well established that testosterone plays a crucial role in maintaining the integrity of epididymal structure and function. However, the role of testosterone in restoring the cellular architecture of the regressed epididymis is not well known. The present study was undertaken to test the hypothesis that testosterone triggers the regressed epididymis by re-expanding existing cells and inducing cell proliferation. Testosterone-dependent epididymal morphology was evaluated in orchidectomized, regressed rats after initiation of treatment with testosterone. Besides that, the proliferative activity of epithelial cells in all regions of the epididymis of the orchidectomized, regressed rats was assessed at 1, 3, 7, and 28 days after testosterone replacement. Epithelial cell proliferation decreased after testosterone withdrawal and increased following testosterone administration. We found that bromodeoxyuridine incorporation and proliferating nuclear antigen expression increased significantly 3 days after testosterone replacement in all regions of the regressed epididymis except in the initial segment. The highest mitotic activity was seen in the corpus epididymidis at 3 days postimplantation. Using specific markers for each cell type, we found no significant changes in the proportion of each cell type compared with the control. We observed labeled nuclei in all epithelial cell types in the control; however, principal cells were the major cell types that responded to testosterone after regression. These observations demonstrate that the mammalian epididymis is not a static tissue without any significant cell renewal, either under control conditions or when androgen exposure is altered, thus providing new insight in the role of androgen in restoration and maintenance of the architecture of the epididymis.
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http://dx.doi.org/10.2164/jandrol.108.006171DOI Listing
April 2009

Androgenic regulation of novel genes in the epididymis.

Asian J Androl 2007 Jul;9(4):545-53

Department of Pharmacology and Therapeutics, McGill University, Montréal, QC H3G1Y6, Canada.

The epididymis is critically dependent on the presence of the testis. Although several hormones, such as retinoids and progestins, and factors secreted directly into the epididymal lumen, such as androgen binding protein and fibroblast growth factor, might play regulatory roles in epididymal function, testosterone (T) and its metabolites, dihydrotestosterone (DHT) and estradiol (E2), are accepted as the primary regulators of epididymal structure and functions, with the former playing the greater role. To ascertain the molecular action of androgens on the epididymis, three complementary approaches were pursued to monitor changes in gene expression in response to different hormonal milieux. The first was to establish changes in gene expression along the epididymis as androgenic support is withdrawn. The second was to determine the sequence of responses that occur in an androgen deprived tissue upon re-administration of the two metabolites of T, DHT and E2. The third was to study the effects of androgen withdrawal and re-administration on gene expression in immortalized murine caput epididymidal principal cells. Specific responses were observed under each of these conditions, with an expected major difference in the panoply of genes expressed upon hormone withdrawal and re-administration; however, some key common features were the common roles of genes in insulin like growth factor/epidermal growth factor and the relatively minor and specific effects of E2 as compared to DHT. Together, these results provide novel insights into the mechanisms of androgen regulation in epididymal principal cells.
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http://dx.doi.org/10.1111/j.1745-7262.2007.00316.xDOI Listing
July 2007

Expression, localization, and regulation of inhibitor of DNA binding (Id) proteins in the rat epididymis.

J Androl 2006 Mar-Apr;27(2):212-24. Epub 2005 Nov 22.

Department of Pharmacology & Therapeutics, McGill University, Montréal, Québec, Canada.

The epididymis is the site in which spermatozoa are matured and stored. Regional differences along the epididymis are essential for the establishment of the microenvironment required for germ cell maturation. Inhibitor of DNA binding (Id) proteins are transcription factors that modulate the functions of basic helix-loop-helix (bHLH) transcription factors and act by binding to and sequestering bHLH proteins; the latter act to regulate cellular proliferation and differentiation. The objectives of this study were to determine the mRNA expression and the immunocytolocalization of Id1, Id2, Id3, and Id4 in the epididymis of adult rats and to determine the Id3 protein expression profile in orchidectomized and in aged animals. We found that, at the mRNA level, Id proteins are expressed in a unique, region-specific manner along the epididymis. Id1 immunoreactivity is specific to myoid cells; the presence of Id2 is observed in clear cells, myoid cells, and in the apical region of principal cells. Id3 immunoreactivity is essentially confined to the nuclei of principal cells and myoid cells, whereas Id4 is observed mainly in myoid and narrow cells. Thus, Ids are localized to different cell types and are differentially expressed, at both the mRNA and protein levels, along the epididymis. Expression of Id3 is differentially regulated in response to orchidectomy along the epididymis. The fact that these regulators of gene expression are expressed in this manner may provide some insight into the differential expression of other genes that lead to region-specific differences along the epididymis, a hallmark of this tissue.
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http://dx.doi.org/10.2164/jandrol.05098DOI Listing
May 2006