Cadmium-induced lipid peroxidation and the status of the antioxidant system in rat tissues.
Cadmium may induce oxidative damage in different tissues by enhancing peroxidation of membrane lipids and altering the antioxidant system of the cells. The peroxidative damage to the cell membrane may cause injury to cellular components due to the interaction of metal ions with the cell organelles. The treatment with Cd (0.4 mg/kg body wt, ip) significantly increased lipid peroxidation (LPO) in heart within 3 h of the Cd injection, while the increase in kidney and liver followed 6 to 12 h after Cd intoxication. The antioxidant enzymes and other antioxidants provide protection to the cells against oxidative damage. The superoxide dismutase (SOD) activity increased in heart, kidney and liver within 24 h of Cd intoxication. The CAT activity increased significantly in heart 9 h after Cd injection; however, no significant change in CAT activity was observed in kidney and liver tissues. The GSH content and the activity of GR decreased in heart, kidney and liver 72 h after Cd administration, which has been suggested to be the cause for increased LPO in the tissues. The hexose monophosphate (HMP) shunt enzymes generate NADPH required for the activity of GR which may affect the GSH content in the tissues. The generalised decrease in glucose 6-phosphate dehydrogenase (G6PDH) and 6 phospho gluconate dehydrogenase (6PGDH) at 9 h followed by an increase in these enzymes in tissues 72 h after Cd intoxication suggest that the production of NADPH by the HMP shunt is required to reduce the oxidative damage. The results show that Cd induced LPO in the tissues and the condition was partially counteracted by the antioxidant system.
Sarkar
S
S
Department of Biochemistry, D.A. University, Indore, India.
Yadav
P
P
Trivedi
R
R
Bansal
A K
AK
Bhatnagar
D
D
D000818:Animals; D002104:Cadmium / Q000633:toxicity*; D002462:Cell Membrane / Q000187:drug effects; D015500:Chloramphenicol O-Acetyltransferase / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D006321:Heart / Q000187:drug effects; D007668:Kidney / Q000166:cytology / Q000187:drug effects / Q000201:enzymology; D015227:Lipid Peroxidation / Q000187:drug effects*; D008099:Liver / Q000166:cytology / Q000187:drug effects / Q000201:enzymology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009206:Myocardium / Q000166:cytology / Q000201:enzymology; D009249:NADP / Q000378:metabolism; D018384:Oxidative Stress; D010734:Phosphogluconate Dehydrogenase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
D017392:Thiobarbituric Acid Reactive Substances; D002104:Cadmium; D008315:Malondialdehyde; D009249:NADP; D010734:Phosphogluconate Dehydrogenase; D005954:Glucosephosphate Dehydrogenase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D015500:Chloramphenicol O-Acetyltransferase; D005982:Glutathione Transferase; D005978:Glutathione