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Role of alpha-tocopherol in cadmium-induced oxidative stress in Wistar rat's blood, liver and brain.
Chem Biol Interact. 2007 Dec 15; 170(3):221-30.CB

Abstract

Cadmium (Cd) a highly toxic metal is considered to be a multitarget toxicant, and it accumulates principally in the liver and kidney after absorption. In vivo studies of mouse and rat liver have shown that apoptosis plays a primary role in Cd-induced hepatotoxicity. However, the detailed mechanisms by which toxic metals such as Cd produce their effects are still largely unknown. The present study aimed at investigating the consequences of exposure to Cd, alpha-tocopherol and their combination on stress biochemical parameters (lipoperoxidation and protein carbonyls levels). Male albino Wistar rats (1 month old) were treated intravenously with cadmium (2 mg CdCl(2)/kg body weight/day), and alpha-tocopherol (100 mg/kg body weight/day), or with alpha-tocopherol+Cd (100 mg Vit E/kg body weight, 2 mg CdCl(2)/kg). The lipoperoxidation was measured by the thiobarbituric acid reactive substances (TBARS) method and oxidatively generated damage to proteins by determining carbonyl (DNPH) levels. Among the hematological parameters measured the haematocrit value and haemoglobin concentration were significantly decreased in the blood of Cd-treated rats. A significant increase was observed in the level of malondialdehyde (MDA) and protein carbonyls in the cadmium exposed group compared to control group (p<0.001), and these values were decreased after administration of alpha-tocopherol (group 4). The activity of lactate dehydrogenase in rat liver and brain showed a significant increase as compared to that found in the control group and significant decrease of catalase and superoxide dismutase activities. In the liver of the Cd-treated group the contents of reduced glutathione were decreased. Our results suggest that cadmium induces an oxidation of cellular lipids and proteins and that administration of alpha-tocopherol can reduce Cd-induced oxidative stress and improve the glutathione level together with other biochemical parameters.

Authors+Show Affiliations

Laboratoire de Physio Pharmacologie, Département de Biologie, Faculté des Sciences, Université de Tlemcen, BP 119, Tlemcen Cedex 13000, Algeria. snemiche@hotmail.comNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17897638

Citation

Nemmiche, Saïd, et al. "Role of Alpha-tocopherol in Cadmium-induced Oxidative Stress in Wistar Rat's Blood, Liver and Brain." Chemico-biological Interactions, vol. 170, no. 3, 2007, pp. 221-30.
Nemmiche S, Chabane-Sari D, Guiraud P. Role of alpha-tocopherol in cadmium-induced oxidative stress in Wistar rat's blood, liver and brain. Chem Biol Interact. 2007;170(3):221-30.
Nemmiche, S., Chabane-Sari, D., & Guiraud, P. (2007). Role of alpha-tocopherol in cadmium-induced oxidative stress in Wistar rat's blood, liver and brain. Chemico-biological Interactions, 170(3), 221-30.
Nemmiche S, Chabane-Sari D, Guiraud P. Role of Alpha-tocopherol in Cadmium-induced Oxidative Stress in Wistar Rat's Blood, Liver and Brain. Chem Biol Interact. 2007 Dec 15;170(3):221-30. PubMed PMID: 17897638.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of alpha-tocopherol in cadmium-induced oxidative stress in Wistar rat's blood, liver and brain. AU - Nemmiche,Saïd, AU - Chabane-Sari,Daoudi, AU - Guiraud,Pascale, Y1 - 2007/08/12/ PY - 2007/03/28/received PY - 2007/07/27/revised PY - 2007/08/07/accepted PY - 2007/9/28/pubmed PY - 2008/2/2/medline PY - 2007/9/28/entrez SP - 221 EP - 30 JF - Chemico-biological interactions JO - Chem Biol Interact VL - 170 IS - 3 N2 - Cadmium (Cd) a highly toxic metal is considered to be a multitarget toxicant, and it accumulates principally in the liver and kidney after absorption. In vivo studies of mouse and rat liver have shown that apoptosis plays a primary role in Cd-induced hepatotoxicity. However, the detailed mechanisms by which toxic metals such as Cd produce their effects are still largely unknown. The present study aimed at investigating the consequences of exposure to Cd, alpha-tocopherol and their combination on stress biochemical parameters (lipoperoxidation and protein carbonyls levels). Male albino Wistar rats (1 month old) were treated intravenously with cadmium (2 mg CdCl(2)/kg body weight/day), and alpha-tocopherol (100 mg/kg body weight/day), or with alpha-tocopherol+Cd (100 mg Vit E/kg body weight, 2 mg CdCl(2)/kg). The lipoperoxidation was measured by the thiobarbituric acid reactive substances (TBARS) method and oxidatively generated damage to proteins by determining carbonyl (DNPH) levels. Among the hematological parameters measured the haematocrit value and haemoglobin concentration were significantly decreased in the blood of Cd-treated rats. A significant increase was observed in the level of malondialdehyde (MDA) and protein carbonyls in the cadmium exposed group compared to control group (p<0.001), and these values were decreased after administration of alpha-tocopherol (group 4). The activity of lactate dehydrogenase in rat liver and brain showed a significant increase as compared to that found in the control group and significant decrease of catalase and superoxide dismutase activities. In the liver of the Cd-treated group the contents of reduced glutathione were decreased. Our results suggest that cadmium induces an oxidation of cellular lipids and proteins and that administration of alpha-tocopherol can reduce Cd-induced oxidative stress and improve the glutathione level together with other biochemical parameters. SN - 0009-2797 UR - https://www.unboundmedicine.com/medline/citation/17897638/Role_of_alpha_tocopherol_in_cadmium_induced_oxidative_stress_in_Wistar_rat's_blood_liver_and_brain_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0009-2797(07)00260-8 DB - PRIME DP - Unbound Medicine ER -