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Deltamethrin-induced oxidative damage and biochemical alterations in rat and its attenuation by Vitamin E.
Toxicology 2006; 227(3):240-7T

Abstract

Deltamethrin is a synthetic pyrethroid insecticide used worldwide in agriculture, home pest control, protection of foodstuff and disease vector control. The objective of this study was to investigate the propensity of deltamethrin to induce oxidative stress and changes in biochemical parameters and enzyme activities in male rats following a short-term (30 days) oral exposure and its possible attenuation by Vitamin E (Vit. E). Rats were assigned to 1 of 4 treatment groups: 0mg Vit. E and 0mg deltamethrin/kg body weight (BW) (control); 100mg Vit. E/kg BW; 1.28mg deltamethrin/kg BW; 100mg Vit. E plus 1.28mg deltamethrin/kg BW. Results obtained showed that deltamethrin significantly (P<0.05) induced thiobarbituric acid-reactive substances (TBARS; the marker of lipid peroxidation) in plasma. The activities of glutathione S-transferase (GST) and superoxide dismutase (SOD) were significantly decreased due to deltamethrin administration. On the other hand, treatment with Vitamin E alone increased the activities of GST and SOD, and decreased the levels of TBARS. Also, Vitamin E alleviated the harmful effect of deltamethrin in the combination group. Enzymatic activities of aminotransferases (AST and ALT), phosphatases (AcP and AlP) and lactate dehydrogenase (LDH) in plasma were significantly increased, while acetylcholinesterase (AChE) was inhibited. Deltamethrin significantly (P<0.05) increased the levels of plasma total lipid (TL), cholesterol, triglyceride (TG), low density lipoprotein (LDL) and very low density lipoprotein (VLDL), while the level of high density lipoprotein (HDL) decreased. Vitamin E alone decreased the levels of lipids and lipoproteins, and alleviated the harmful effects of deltamethrin. Concentrations of glucose, urea, creatinine and total bilirubin were increased. While, plasma total protein (TP), albumin (A) and globulin (G) were significantly (P<0.05) decreased. The present study revealed that the presence of Vitamin E could diminish the adverse effects of deltamethrin on most of biochemical parameters, lipid peroxidation and enzyme activities in rats.

Authors+Show Affiliations

Department of Environmental Studies, Institute of Graduate Studies and Research, Alexandria University, 163, Horreya Avenue, P.O. Box 832, Alexandria 21526, Egypt. mokhtar_yousef@yahoo.comNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16978760

Citation

Yousef, Mokhtar I., et al. "Deltamethrin-induced Oxidative Damage and Biochemical Alterations in Rat and Its Attenuation By Vitamin E." Toxicology, vol. 227, no. 3, 2006, pp. 240-7.
Yousef MI, Awad TI, Mohamed EH. Deltamethrin-induced oxidative damage and biochemical alterations in rat and its attenuation by Vitamin E. Toxicology. 2006;227(3):240-7.
Yousef, M. I., Awad, T. I., & Mohamed, E. H. (2006). Deltamethrin-induced oxidative damage and biochemical alterations in rat and its attenuation by Vitamin E. Toxicology, 227(3), pp. 240-7.
Yousef MI, Awad TI, Mohamed EH. Deltamethrin-induced Oxidative Damage and Biochemical Alterations in Rat and Its Attenuation By Vitamin E. Toxicology. 2006 Oct 29;227(3):240-7. PubMed PMID: 16978760.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Deltamethrin-induced oxidative damage and biochemical alterations in rat and its attenuation by Vitamin E. AU - Yousef,Mokhtar I, AU - Awad,Talaat I, AU - Mohamed,Edriss H, Y1 - 2006/08/14/ PY - 2006/05/31/received PY - 2006/08/03/revised PY - 2006/08/08/accepted PY - 2006/9/19/pubmed PY - 2006/11/14/medline PY - 2006/9/19/entrez SP - 240 EP - 7 JF - Toxicology JO - Toxicology VL - 227 IS - 3 N2 - Deltamethrin is a synthetic pyrethroid insecticide used worldwide in agriculture, home pest control, protection of foodstuff and disease vector control. The objective of this study was to investigate the propensity of deltamethrin to induce oxidative stress and changes in biochemical parameters and enzyme activities in male rats following a short-term (30 days) oral exposure and its possible attenuation by Vitamin E (Vit. E). Rats were assigned to 1 of 4 treatment groups: 0mg Vit. E and 0mg deltamethrin/kg body weight (BW) (control); 100mg Vit. E/kg BW; 1.28mg deltamethrin/kg BW; 100mg Vit. E plus 1.28mg deltamethrin/kg BW. Results obtained showed that deltamethrin significantly (P<0.05) induced thiobarbituric acid-reactive substances (TBARS; the marker of lipid peroxidation) in plasma. The activities of glutathione S-transferase (GST) and superoxide dismutase (SOD) were significantly decreased due to deltamethrin administration. On the other hand, treatment with Vitamin E alone increased the activities of GST and SOD, and decreased the levels of TBARS. Also, Vitamin E alleviated the harmful effect of deltamethrin in the combination group. Enzymatic activities of aminotransferases (AST and ALT), phosphatases (AcP and AlP) and lactate dehydrogenase (LDH) in plasma were significantly increased, while acetylcholinesterase (AChE) was inhibited. Deltamethrin significantly (P<0.05) increased the levels of plasma total lipid (TL), cholesterol, triglyceride (TG), low density lipoprotein (LDL) and very low density lipoprotein (VLDL), while the level of high density lipoprotein (HDL) decreased. Vitamin E alone decreased the levels of lipids and lipoproteins, and alleviated the harmful effects of deltamethrin. Concentrations of glucose, urea, creatinine and total bilirubin were increased. While, plasma total protein (TP), albumin (A) and globulin (G) were significantly (P<0.05) decreased. The present study revealed that the presence of Vitamin E could diminish the adverse effects of deltamethrin on most of biochemical parameters, lipid peroxidation and enzyme activities in rats. SN - 0300-483X UR - https://www.unboundmedicine.com/medline/citation/16978760/Deltamethrin_induced_oxidative_damage_and_biochemical_alterations_in_rat_and_its_attenuation_by_Vitamin_E_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0300-483X(06)00502-6 DB - PRIME DP - Unbound Medicine ER -