4.4 Article

Mitigative role of garlic and vitamin E against cytotoxic, genotoxic, and apoptotic effects of lead acetate and mercury chloride on WI-38 cells

Journal

PHARMACOLOGICAL REPORTS
Volume 70, Issue 4, Pages 804-811

Publisher

POLISH ACAD SCIENCES INST PHARMACOLOGY
DOI: 10.1016/j.pharep.2018.02.009

Keywords

Garlic; Vitamin E; WI-38; Lead acetate; Mercury chloride; Genotoxicity; Cytotoxicity

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Background: Lead acetate (Led) and mercury chloride (Mer) represent important ecological and public health concerns due to their hazardous toxicities. Naturally found products play a vital role in chemopreventive agent innovation. The current study aimed to assess the modifying effect of garlic (Gar) and/or vitamin E (Vit E) against the half-maximal inhibitory concentration (IC50) Led and/or Mer-induced cytotoxic, genotoxic and apoptotic effects. Methods: Human lung cells (WI-38) were pretreated with Gar and/or Vit E for 24 h and then treated with Led and/or Mer either alone or with their combination for 24 h. Cytotoxicity of Led and Mer and the viability of Gar and Vit E were assessed using MTT assay. The alkaline comet assay was used to assess DNA damage, whereas QRT-PCR was performed to evaluate p53, Bax, and Bcl2 mRNA-expression. Results: The results of this study showed that IC50 of Led was (732.72 mu g/mL) and for Mer was (885.83 mu g/mL), while cell viability effective dose for Gar was (300 mu g/mL) and for Vit E was (26,800 mu g/mL). Treating cells with the IC50-concentration of Led or Mer or their combination using half IC50 of both of them induced severe DNA-damage. Bax-expression was increased, while p53 and Bcl2-expressions were decreased. Pretreatment of cells with Gar and/or Vit E ameliorated the previous alternations. Conclusions: Led and Mer can induce oxidative stress and change the expressions of apoptosis-related proteins in WI-38 cells. Gar and Vit E may be promising protective candidate agent against the toxic effect of heavy metals. (C) 2018 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier B.V. All rights reserved.

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