l-arginine ameliorated mitochondrial oxidative damage induced by sub-chronic exposure to cadmium in mice kidney

Background: cadmium is a heavy metal that can cause various injuries in the body, includingnephrotoxicity. l-arginine is a metal chelator that can prevent oxidative damage caused byoxygen free radicals.objectives: this study aimed to investigate the effect of l-arginine in inhibiting mitochondrialtoxicity 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 (normalsaline), cadmium (2 mg/kg), cadmium (2 mg/kg) plus three doses of l-arginine (50, 100, and 200mg/kg) and finally cadmium (2 mg/kg) plus vitamin c (500 mg/kg). after 42 days, the animalswere anesthetized with ketamine/xylazine. their kidney tissues were removed, and mitochondrialfractions 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 andoxidation 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 mitochondrialdamage (p<0.05). furthermore, a significant reduction in serum bun and cr were observedin l-arginine received group (p<0.05).conclusion: the results showed that l-arginine has significant protective effects againstcadmium-induced renal toxicity in male mice.