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، جلد ۷، شماره ۲، صفحات ۷۹-۸۶
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| عنوان فارسی |
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| چکیده فارسی مقاله |
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| کلیدواژه‌های فارسی مقاله |
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| عنوان انگلیسی |
L-arginine Ameliorated Mitochondrial Oxidative Damage Induced by Sub-chronic Exposure to Cadmium in Mice Kidney |
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| چکیده انگلیسی مقاله |
Background: Cadmium is a heavy metal that can cause various injuries in the body, including nephrotoxicity. L-Arginine is a metal chelator that can prevent oxidative damage caused by oxygen free radicals. Objectives: This study aimed to investigate the effect of L-arginine in inhibiting mitochondrial toxicity induced by subchronic cadmium exposure in the kidney of male mice. Methods: A total of 42 male mice were randomly divided into six groups (n=6): control (normal saline), cadmium (2 mg/kg), cadmium (2 mg/kg) plus three doses of L-arginine (50, 100, and 200 mg/kg) and finally cadmium (2 mg/kg) plus vitamin C (500 mg/kg). After 42 days, the animals were anesthetized with ketamine/xylazine. Their kidney tissues were removed, and mitochondrial fractions were isolated. Oxidative stress factors and mitochondrial damage parameters (MTT, swelling, and mitochondrial membrane potential) were measured in renal isolated mitochondria. Also, evaluation of Blood Urea Nitrogen (BUN) and Creatinine (Cr) tests were done. Results: Significant rise in BUN and Cr were observed in cadmium-treated mice (P< 0.05). Cadmium enhanced oxidative stress in the kidney via increasing lipid peroxidation and oxidation of protein and glutathione. It caused significant mitochondrial dysfunction, mitochondrial membrane potential collapse, and swelling in isolated mitochondria (P< 0.05). L-Arginine significantly ameliorated cadmium-induced oxidative stress and mitochondrial damage (P< 0.05). Furthermore, a significant reduction in serum BUN and Cr were observed in L-arginine received group (P< 0.05). Conclusion: The results showed that L-arginine has significant protective effects against cadmium-induced renal toxicity in male mice. |
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| کلیدواژه‌های انگلیسی مقاله |
Cadmium, L-Arginine, Kidney, Oxidative stress, Mitochondria |
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| نویسندگان مقاله |
| Fatemeh Shaki
Pharmaceutical Sciences Research Center, Hemoglobinopathy Institute, Mazandaran University of Medical Sciences, Sari, Iran.
| Melika Teymoori
Department of Toxicology and Pharmacology, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran.
| Farzaneh Sadat Motafeghi
Department of Toxicology and Pharmacology, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran.
| Nasibeh Hemmati
Pharmaceutical Sciences Research Center, Hemoglobinopathy Institute, Mazandaran University of Medical Sciences, Sari, Iran.
| Milad Arab-Nozari
Department of Toxicology and Pharmacology, Faculty of Pharmacy, Ayatollah Amoli Branch, Islamic Azad University, Amol, Iran.
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| نشانی اینترنتی |
http://pbr.mazums.ac.ir/browse.php?a_code=A-10-48-4&slc_lang=en&sid=1 |
| فایل مقاله |
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| کد مقاله (doi) |
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| زبان مقاله منتشر شده |
en |
| موضوعات مقاله منتشر شده |
سم شناسی |
| نوع مقاله منتشر شده |
پژوهشی |
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