Protective Role of S-Adenosyl Methionine (SAMe) in Cadmium Induced Toxicopathological Changes in Wistar Rats


Abstract

Cadmium is considered to be one of the most toxic substances in the environment due to its wide range of organ toxicity and long elimination half-life. SAMe is recognized as the major methyl-donor for essential methylation reactions that occur in all living organisms. SAMe has been increasingly utilized as a therapeutic agent in liver and neurological disorders recently. The present study has been devised to explore the alleviating effects of SAMe in cadmium induced toxicopathological changes in rats. The rats were divided into four experimental groups: group I formed the control, group II animals were given cadmium chloride @ 200ppm in distilled water, orally, group III animals were given SAMe @ 1 mg/kg body weight, orally and group IV were given both CdCl2 and SAMe. Six rats from each group were humanely sacrificed at 30th, 60th and 90th day. The quantitative data of body weight, absolute organ weight, cadmium content and oxidative stress parameters was analyzed by Duncan's multiple range tests The group II animals showed most of the pathological changes compared to the rest of the group. The magnitude of lesions in various organs was lesser in group IV where SAMe was given. The severity of lesions increased with the advancement of experiment; most severe pathological changes occurring on the 90th day. The level of cadmium residue in liver and kidneys of rats was also found to be increasing with the time in group II and IV; with group IV showing a relatively lesser increase. Similarly the evaluation of oxidative stress parameters reflected the detrimental effect of cadmium in group II and an alleviating effect of SAMe in group IV. Based on the results obtained, SAMe is found to alleviate the toxicopathological effects of cadmium in rats which needs to be further explored.

Keywords

Cadmium, S-Adenosyl Methionine, Rats, Toxicopathology.

Subject Discipline

Pharmacy and Pharmacology

Full Text:

Refbacks

  • There are currently no refbacks.