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Cadmium-induced lipid peroxidation and the status of the antioxidant system in rat tissues.

Abstract

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.

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  • Authors+Show Affiliations

    ,

    Department of Biochemistry, D.A. University, Indore, India.

    , , ,

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    MeSH

    Animals
    Cadmium
    Cell Membrane
    Chloramphenicol O-Acetyltransferase
    Dose-Response Relationship, Drug
    Glucosephosphate Dehydrogenase
    Glutathione
    Glutathione Peroxidase
    Glutathione Reductase
    Glutathione Transferase
    Heart
    Kidney
    Lipid Peroxidation
    Liver
    Male
    Malondialdehyde
    Myocardium
    NADP
    Oxidative Stress
    Phosphogluconate Dehydrogenase
    Rats
    Rats, Wistar
    Superoxide Dismutase
    Thiobarbituric Acid Reactive Substances

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    8605602

    Citation

    Sarkar, S, et al. "Cadmium-induced Lipid Peroxidation and the Status of the Antioxidant System in Rat Tissues." Journal of Trace Elements in Medicine and Biology : Organ of the Society for Minerals and Trace Elements (GMS), vol. 9, no. 3, 1995, pp. 144-9.
    Sarkar S, Yadav P, Trivedi R, et al. Cadmium-induced lipid peroxidation and the status of the antioxidant system in rat tissues. J Trace Elem Med Biol. 1995;9(3):144-9.
    Sarkar, S., Yadav, P., Trivedi, R., Bansal, A. K., & Bhatnagar, D. (1995). Cadmium-induced lipid peroxidation and the status of the antioxidant system in rat tissues. Journal of Trace Elements in Medicine and Biology : Organ of the Society for Minerals and Trace Elements (GMS), 9(3), pp. 144-9.
    Sarkar S, et al. Cadmium-induced Lipid Peroxidation and the Status of the Antioxidant System in Rat Tissues. J Trace Elem Med Biol. 1995;9(3):144-9. PubMed PMID: 8605602.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Cadmium-induced lipid peroxidation and the status of the antioxidant system in rat tissues. AU - Sarkar,S, AU - Yadav,P, AU - Trivedi,R, AU - Bansal,A K, AU - Bhatnagar,D, PY - 1995/10/1/pubmed PY - 1995/10/1/medline PY - 1995/10/1/entrez SP - 144 EP - 9 JF - Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) JO - J Trace Elem Med Biol VL - 9 IS - 3 N2 - 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. SN - 0946-672X UR - https://www.unboundmedicine.com/medline/citation/8605602/Cadmium_induced_lipid_peroxidation_and_the_status_of_the_antioxidant_system_in_rat_tissues_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0946-672X(11)80038-6 DB - PRIME DP - Unbound Medicine ER -