Combined exposure to cadmium and fluoride non-toxic levels leads to nephrotoxicity in rats via induction of oxidative stress
محل انتشار: پانزدهمین همایش سراسری سم شناسی ایران
سال انتشار: 1398
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 407
نسخه کامل این مقاله ارائه نشده است و در دسترس نمی باشد
- صدور گواهی نمایه سازی
- من نویسنده این مقاله هستم
استخراج به نرم افزارهای پژوهشی:
شناسه ملی سند علمی:
TOXICOLOGY15_106
تاریخ نمایه سازی: 15 بهمن 1398
چکیده مقاله:
Introduction: Humans are encountered to mixtures of pollutants in the environment. Most studies only focused on the effects of a single pollutant and exposure to high doses. Cadmim (Cd) and Fluoride (F) are two common water pollutants. In this study, we evaluated the combination effects of non-toxic doses of F and Cd in the kidney tissue of male wistar rats.Methods: 24 rats were randomly divided in to four groups as follows: control (drinking water), F (30 ppm sodium fluoride), Cd (40 ppm cadmium chloride) and F+Cd control (30 ppm sodium fluoride plus 40 ppm cadmium chloride) that were dissolved in drinking. After 42 days, rats were anesthetized and kidney tissues were separated and then oxidative stress markers were evaluated. Also, blood samples were collected for assessment of blood urea nitrogen (BUN), creatinine (Cr).Results: significant increase in oxidative stress markers including reactive oxygen spices, lipid peroxidation, protein carbonyl were detected following co-exposure to F and Cd in comparison to control and individual groups. Also, marked decline in renal glutathione and superoxide dismutase levels (two important endogenous antioxidants) were assessed in rats that received combination of F and Cd. Furthermore, BUN and Cr levels were significantly raised in the serum samples of F+Cd threated group in comparison to F or Cd alone and also control group. While, Cd and F alone didn’t induce any significant changes in evaluated factors compared to control groups.Conclusion: Co-exposure to F and Cd definitely results in a synergism of the nephrotoxic effects via induction of oxidative stress pathway.
کلیدواژه ها:
نویسندگان
Milad Arab-Nozari
Student Research Committee, Mazandaran University of Medical Sciences, Sari, Iran- Department of Toxicology and Pharmacology, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran
Fatemeh Shaki
Department of Toxicology and Pharmacology, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran- Pharmaceutical Science Research Center, Hemoglobinopathy Institute, Mazandaran University of Medical Sciences, Sari, Iran
Nematollah Ahangar
Department of Pharmacology, Faculty of Medicine, Guilan University of Medical Sciences, Rasht, Iran