Solanum torvum Swartz. fruit attenuates cadmium-induced liver and kidney damage through modulation of oxidative stress and glycosylation

Abstract

Increased levels of environmental pollutants are linked to almost all human disorders; the efficient method to manage the human health is through naturally available dietary molecule. Solanum torvum (ST) Swartz (Solanaceae) commonly called Turkey Berry is found in Africa, Asia, and South America. Its fruit, part of traditional Indian cuisine, is a widely consumed nutritious herb, acclaimed for its medicinal value. ST aqueous extract (STAe) (250, 500, and 1000 mg/kg b.w., 6 days; oral) against acute Cadmium (Cd) (6.3 mg/kg b.w., single dose; oral) toxicity was evaluated in rats. Protective effect was assessed using serum markers, tissue antioxidants, oxidant derivatives, glycoprotein, and histopathological studies. The activities of serum marker enzymes were increased (40-60 %); antioxidant enzymes such as SOD and CAT, GSH, and its metabolic enzyme activities were decreased (50-80 %) in the liver and kidney upon Cd intoxication. During STAe pre-treatment, at doses of 250 and 500 mg/kg b.w., the above changes were brought to near normal (25-63 %). Tissue 4-hydroxynonenal, 3-nitrotyrosine, and protein carbonyls were increased (8-15 fold) in Cd-alone-treated rats, whereas pre-supplementation of STAe significantly decreased their levels and inhibited the protein glycosylation effectively. The pharmacological effect of STAe was confirmed by histopathological observations. Based on previous literature and present investigation, we conclude that ST may serve as a potential functional food against environmental contaminant such as heavy metal-induced oxidative stress.

Effect of Aqueous Extract Cyperus rotundus Tubers as Antioxidant on Liver and Kidney Functions in Albino Males Rats Exposed to Cadmium Chloride Toxic

“…The damage of cadmium chloride in the liver and kidneys, induced the over-generated ROS and diminished antioxidant enzymes lead to uncontrolled oxidative stress. Oxidative stress stimulates the damages of DNA, lipids, proteins and other cellular biomolecules, as well as promoting the interruption of cellular redox homeostasis, the cellular apoptosis and the abnormal activation of signaling pathways (36,37). The reason for the increase in the concentration of MDA in animals exposed to oxidtive stress is the result of treatment with cadmium chloride, which may result in the formation of free radicals that attack the fat and its compounds in the body, especially in the cellular membranes and work on oxidation and damage.…”

Oleanolic Acid, a Prospective Protective Agent Against Brain Energy Metabolism and Oxidative Dysfunctions Following Hexavalent Chromium Exposure in Mice

“…Similar observation was also noted in the present study where chromium exposure significantly elevated carbonylated protein content in the brain tissue of mice. In addition, heavy metals also induce abnormal glycosylation of tissue proteins [54]. Uncharacterized glycosylated or post-translated proteins lose their ability to achieve programmed function of cellular integrity [55] and may thereby encourage tissue metabolic disorders.…”

Modulation of Cadmium Induced Apoptotic, Cancer and Inflammation Related Cytokines by Diallyl Disulfide in Rat Liver Cells

“…In the same study, it was reported that individuals in the top quartile of creatinine-corrected urinary Cd had over a threefold increased risk of liver disease mortality. The liver injury is characterized by increased serum levels of hepatic transaminases and massive necrosis of hepatocytes [10]. In addition to the induction of necrosis, cadmium has been reported to induce apoptosis in liver cells [11].…”