Effect of Ramadan fasting on markers of oxidative stress and serum biochemical markers of cellular damage in healthy subjects.

Authors:
Mr Amjad Jarrar, M Sc.
Mr Amjad Jarrar, M Sc.
United Arab Emirates University
Instructor
Human Nutrition
Alain, Abu Dhabi | United Arab Emirates
Hosam Habib
Hosam Habib
United Arab Emirates University
United Arab Emirates

Ann Nutr Metab 2008 14;53(3-4):175-81. Epub 2008 Nov 14.

Department of Nutrition and Health, College of Food and Agriculture, United Arab Emirates University, Al Ain, United Arab Emirates.

Background/aims: Ramadan is a holy month for Muslims during which they abstain from eating, drinking and smoking from dawn to sunset. This makes Ramadan a unique model for studying the effects of altered meal patterns in humans. The aim of this study was to determine the effect of Ramadan fasting on markers of oxidative stress and serum biochemical markers of cellular damage in healthy subjects.

Methods: Fourteen healthy volunteers (9 men and 5 women aged 25-58 years) who fasted during Ramadan participated in the study. Blood sampling was conducted 2 days before Ramadan and on days 14 and 28 of Ramadan. The following were measured: (1) in serum, malondialdehyde (MDA), aspartate aminotransferase, alanine aminotransferase, creatine kinase, alkaline phosphatase, lactate dehydrogenase, blood urea nitrogen, total proteins, uric acid, albumin, glucose, triglycerides and total cholesterol; (2) in plasma, protein-bound carbonyls, alpha-tocopherol, gamma-tocopherol, retinol, vitamin C and carotenoids, and (3) in erythrocytes, MDA, glutathione, glutathione peroxidase and catalase.

Results: Erythrocyte MDA, serum glucose and triglycerides and plasma total carotenoids were significantly lower (p<0.05) on day 28 of Ramadan compared to before Ramadan. The rest of the variables were not significantly altered by Ramadan fasting.

Conclusion: The results obtained indicate that with the exception of a slight reduction in lipid peroxidative damage in erythrocytes, Ramadan fasting does not alter oxidative stress parameters or biochemical markers of cellular damage in healthy subjects.

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Source
http://dx.doi.org/10.1159/000172979DOI Listing
April 2009
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