L-arginine Ameliorated Mitochondrial Oxidative Damage Induced by Sub-chronic Exposure to Cadmium in Mice Kidney

Abstract

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.