Abstract

This study was designed to assess the effect to apple cider vinegar (ACV) on oxidative stress biomarkers in male and female Wistar rats exposed to chronic restraint stress. Severe and persistent stress elevates reactive oxygen species (ROS) production by metabolic and physiological processes; causing cellular damage. Thirty (30) Adult Wistar rats of both sexes weighing about 150 - 200 g were divided into 3 groups each consisting of a male and female subgroup and given the following treatments once a day for 21 days: Normal control group received 0.5 ml distilled water orally, the restraint stress (RS) group was exposed to chronic restraint stress 6 hours daily while the Apple cider vinegar (ACV)-treated group received 4 ml/kg of apple cider vinegar orally in addition to chronic restraint stress 6 hours daily. The rats were sacrificed after the experimental period and blood was collected via cardiac puncture for assessing oxidative stress biomarkers. ACV (4 ml/kg) treatment decreased lipid peroxidation (MDA) and serum catalase (CAT) activity while upregulating endogenous superoxide dismutase (SOD) activity. The findings of this study show that the female Wistar rats are more predisposed to the antioxidant effect of ACV than the males.

Highlights

  • Thirty (30) Adult Wistar rats of both sexes weighing about 150 - 200 g were divided into 3 groups each consisting of a male and female subgroup and given the following treatments once a day for 21 days: Normal control group received 0.5 ml distilled water orally, the restraint stress (RS) group was exposed to chronic restraint stress 6 hours daily while the Apple cider vinegar (ACV)-treated group received 4 ml/kg of apple cider vinegar orally in addition to chronic restraint stress 6 hours daily

  • The findings of this study show that the female Wistar rats are more predisposed to the antioxidant effect of ACV than the males

  • Physical restraint is a well-known stress model, which increases oxidative processes leading to the generation of reactive oxygen species which may propagate the initial attack on lipid rich membranes to cause lipid peroxidation [3]

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Summary

Introduction

Severe and persistent stress elevates reactive oxygen species (ROS) production by metabolic and physiological processes; causing cellular damage [2]. Physical restraint is a well-known stress model, which increases oxidative processes leading to the generation of reactive oxygen species which may propagate the initial attack on lipid rich membranes to cause lipid peroxidation [3]. Excessive reactive oxygen species production resulting from stress hormones leads to an increase in lipid peroxidation of the cellular structures which play an important role in pathogenesis of degenerative diseases, such as atherosclerosis, oxidative damage to DNA, and carcinogenesis. Reactive oxygen species are kept at physiologically optimal levels by the endogenous antioxidant defense systems as well as natural exogenous antioxidants derived from the diet [4]. The endogenous antioxidant system includes the array of antioxidant enzymes; cellular and mitochondrial superoxide dismutases (copper/zinc (CuZnSOD) and Mn2+-dependent superoxide dismutase (MnSOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR), and non-enzymatic antioxidants such as glutathione (GSH)

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