Abstract

Hexavalent chromium Cr(VI) is a very strong oxidant which consequently causes high cytotoxicity through oxidative stress. Prevention of Cr(VI)-induced cellular damage has been sought in this study in aqueous and methanolic extracts of Lawsonia inermis Linn. (Lythraceae), commonly known as Henna. The extracts showed significant (P < .05) potential in scavenging free radicals (DPPH• and ABTS•+) and Fe3+, and in inhibiting lipid peroxidation. DNA damage caused by exposure of pBR322 to Cr(VI)-UV is markedly inhibited by both extracts in varying degrees. A distinct decline in Cr(VI)-induced cytotoxicity was noticed in MDA-MB-435S (human breast carcinoma) cells with an increase in dosage of both extracts individually. Furthermore, both extracts proved to contain a high content of phenolic compounds which were found to have a strong and significant (P < .05) positive correlation to the radical scavenging potential, lipid peroxidation inhibition capacity and cyto-protective efficiency against Cr(VI)-induced oxidative cellular damage. HPLC analysis identified some of the major phenolic compounds in both extracts, which might be responsible for the antioxidant potential and the properties of DNA and cyto-protection. This study contributes to the search for natural resources that might yield potent therapeutic drugs against Cr(VI)-induced oxidative cell damage.

Highlights

  • Hexavalent chromium [Cr(VI)] is the most toxic and mutagenic heavy metal in biological systems [1]

  • Radical scavenging efficiency was considerably higher in the ABTS assay in comparison to Results of the Ferric Reducing Antioxidant Property (FRAP) assay (Figure 1(c)) showed that the aqueous extract was a stronger Fe3+-reductant than the methanolic extract

  • Intracellular and membrane lipids, when subjected to considerable oxidative stress, lose a hydrogen atom from an unsaturated fatty acyl chain, initiating lipid peroxidation which propagates as a chain reaction

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Summary

Introduction

Hexavalent chromium [Cr(VI)] is the most toxic and mutagenic heavy metal in biological systems [1]. It exists as oxo-species such as CrO3 and CrO24−, which are robustly oxidizing [2], leading to excessive cytotoxicity that in turn may cause dermal damage, gastrointestinal bleeding, renal failure, intravascular hemolysis, liver damage, coma and even death [3]. Oxidative damage is associated with the generation of free radicals in cells exposed to Cr(VI) ion, and a propensity of cells to develop mutations in response to Cr(VI)-induced oxidative damage has been reported [11, 12]. Sources of Cr(VI) toxicity are broadly classified into occupational and non-occupational exposure types. Non-occupational sources of exposure include food, air and water [7]

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