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.

Administration of combined exogenous L-arginine and ascorbic acid attenuates potassium bromate-induced renal and hepatic toxicity

“…The present study has demonstrated that administration of exogenous L-arginine in combination with ascorbic acid is beneficial in potassium bromate-induced organ damage in rats. Our results agree with those of previous studies which reported that doses of ascorbic acid or L-arginine between 500 and 1000 mg/kg body weight restored induced alterations in biochemical indices of kidney function in rodents, and that histological aberrations induced in renal tissues were also ameliorated (Kandhare et al, 2015;Shaki et al, 2021). The probable mechanism of action of L-arginine is its antioxidative effect elicited by direct chemical interaction with superoxide anion (Liang et al, 2018, Li et al, 2022.…”

Pomegranate peel extract, N-Acetylcysteine and their combination with Ornipural alleviate Cadmium-induced toxicity in rats

“…N-acetylcysteine + Orn treatment may have reduced Cd-induced liver DNA damage. Antioxidant properties of Orn (especially betaine), PPE and NAC may have prevented oxidative DNA damage in the liver tissue [ 25 , 26 , 36 , 41 , 48 , 63 , 67 ].…”

“…Ornipural (1 mL/kg) treatments on some biomarkers in liver tissue toxicity of Cd (mg/kg) in rats (Mean ± SEM) The liver MDA levels decreased in concomitant administration of NAC and NAC + Orn with Cd (P˂0.05, Table 1). Ornipural has antioxidant ingredients such as L-arginine, betaine, and methionine, which positively affect antioxidant enzymes [41,63]. N-acetylcysteine increases the level of intracellular antioxidant enzymes such as GSH and has scavenging effects on oxidative radicals [48].…”

“…L-arginine is a necessary substrate for the production of nitric oxide (NO), which aids in important role in various physiological processes such as neurotransmission, cytotoxicity and immunity [ 28 ]. Although it is defined that L-arginine may be protective against Cd toxicity due to its antioxidant properties [ 63 ], its effects on Cd toxicity are not well understood.…”

Oxidative stress in liver of streptozotocin-induced diabetic mice fed a high-fat diet: A treatment role of Artemisia annua L.

“…MDA is the end product of the membrane lipid peroxidation produced by action of free radicals (Shokrzadeh et al 2015;Shaki et al 2021). ROS are products of normal metabolism in body (Teow et al 2007;Iqbal et al 2012) that is excessively generated by a prolonged hyperglycemia (Taile et al 2020).…”