Tomato Extract Antagonizes Cadmium-Induced Hepatotoxicity and Nephrotoxicity in Mice and HepG2 Cells: Inhibition of Oxidative Damage and Apoptosis

Abstract

Cadmium (Cd), a highly toxic heavy metal, accumulates in the liver and kidneys in the human body by several routes. Tomatoes and related processed food possess multiple physiological functions such as antioxidation, antiinflammation, and anticancer. Herein, to investigate whether tomato extract (TE) can protect against cadmium chloride (CdCl2)-induced oxidative damage in the liver and kidneys, the oxidative damage models were established in vitro and in vivo, and the control group and TE intervention groups were also set up. A significant elevation was observed in Cd concentration and the level of alanine transaminase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), creatinine (CR), and uric acid (UA) in the serum of CdCl2-treated rats compared with the control group, by contrast, these values were reduced following TE intervention. Moreover, it was found that exposure to CdCl2 decreased the superoxide dismutase (SOD) activity, glutathione (GSH) level, and catalase (CAT) activity and raised the malondialdehyde (MDA) level in serum, liver tissues, kidney tissues, and HepG2 cells, which can be reversed by TE to mitigate the oxidative damage. In addition, TE exerted an inhibitory effect on cell apoptosis in both liver and kidneys brought on by CdCl2 intoxication, as manifested by the downregulation of Caspase-3 protein and the up-regulation of B-cell lymphoma gene 2 (Bcl-2) protein after TE treatment. Altogether, our study reinforces previous findings that CdCl2 exposure disrupted the redox homeostasis, leading to oxidative damage in both liver and kidneys. More importantly, our findings suggest that the hepatorenal protective effect of TE against CdCl2 toxicity is implicated in the inhibition of oxidative stress and apoptosis.