Catechin supplementation prevents kidney damage in rats repeatedly exposed to cadmium through mitochondrial protection

Abstract

Nephrotoxicity is recognized as a serious disorder affected by chronic cadmium exposure. Imbalance between radical generation and elimination is considered a critical factor involved in the initiation and progression of renal injury caused by this heavy metal. The present study investigated the possible protection by catechin, a natural phenolic antioxidant, against cadmium nephrotoxicity and elucidated its potential mechanism. Male Wistar rats were assigned to receive vehicle, cadmium (CdCl 2 mg/kg, i.p.) and cadmium plus catechin (25, 50, and 100 mg/kg, orally, respectively). After 4 weeks of treatment, rats exposed to cadmium demonstrated a marked rise in blood urea nitrogen and creatinine, a fall in creatinine clearance, and renal pathologies like severe tubular damage, apoptosis, and abnormal mitochondrial structure. Significant increases in malondialdehyde, nitric oxide, and tumor necrosis factor-alpha, while reductions in antioxidant thiols, superoxide dismutase, and catalase, were also detected in the kidney tissues of cadmium-intoxicated rats. These alterations were associated with mitochondrial dysfunction as supported by an increase in mitochondrial reactive oxygen species production and a decline in mitochondrial membrane potential. Treatment with catechin significantly attenuated all the changes caused by cadmium. These findings suggest that catechin effectively protects the kidney against toxic effect of cadmium, presumably through its antioxidant, anti-inflammation, and mitochondrial protection. The study outcomes not only add evidence to reinforce the medical benefits of catechin but also, most importantly, give rise to a prospect of developing renal preventive strategy for individuals who are at risk of cadmium contamination by means of catechin supplementation.

Nutrients, Nutraceuticals, and Xenobiotics Affecting Renal Health

“…In addition, EGCG counteracted the UUO effects by normalizing the antioxidant and inflammatory activity [ 121 ]. In another very recent study, catechin administration at different dosages after cadmium exposure significantly attenuated the nephrotoxic effects of cadmium exposure by reducing oxidative stress and inflammation and by protecting the renal mitochondrial structure and function [ 122 ]. A protective role of EGCG in the development of diabetic nephropathy in mice has also been reported [ 123 , 124 , 125 , 126 , 127 ], inducing the upregulation of the nuclear factor erythroid 2-related factor 2 (NRF2), which plays a key role in cellular defense against diabetes-induced oxidative stress [ 127 ].…”

The Regulation of Host Intestinal Microbiota by Polyphenols in the Development and Prevention of Chronic Kidney Disease

“…These alterations have often been associated with mitochondrial dysfunction, supported by an increase in the production of mitochondrial ROS and a decrease in mitochondrial membrane potential. These results indicated that, probably by means of its antioxidant, anti-inflammatory, and mitochondrial defense abilities, catechin effectively protected the kidney against cadmium toxicity (101). In another example, histopathology showed degenerative changes in glomeruli and tubules 2 weeks after administration of gentamicin to rats.…”

Combined effect of cadmium and noise on rat’s kidney

“…Abdel-Moneim and Said observed cadmium produced a significant decreased the antioxidant enzymes activity in kidney tissue which might be the effect of the overproduction of reactive oxygen species (ROS) (23). Evidence supports that production of oxidative stress is the most responsible reason for cadmium toxicity (22)(23)(24)(25)(26).…”