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Tannic acid alleviates lead acetate-induced neurochemical perturbations in rat brain.

Abstract：

:Oxidative stress has been projected as a promising mechanism involved in lead exposure. The lead predisposition catalyzes oxidative reactions and generates reactive oxygen species. The present study was carried out to investigate the effect of oral administration of tannic acid (TA) on behavioral deficit, antioxidative deterioration induced by lead acetate (LA) exposure on experimental rat brain. Male Wistar rats were treated with 50mg/kg body weight of LA and TA for three times a week for two weeks. Our data showed LA-induced profound elevation of ROS production and oxidative stress, as evidenced by increased levels of oxidative stress markers such as lipid peroxidation and protein carbonyl observed in LA treated rats, whereas significant depletion in the activity of non-enzymatic antioxidants, enzymatic antioxidants, neurotoxicity biomarker and histological changes were observed in LA treated rat brain. However, TA administration restored antioxidant status of brain significantly when compared to control. Our results demonstrate that TA exhibits potent antioxidant properties and suppresses oxidative damages in rat brain induced by LA treatment. These findings were further supported by the neurotoxicity biomarker and histopathological findings in the brain tissue showed that TA protected tissue from deleterious effects of LA exposure. It is concluded, these data suggest that LA induces oxidative stress and supplementation of TA has a powerful antioxidant effect, and it protected rat brain from poisonous effect of LA exposure in experimental rat.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Ashafaq M,Tabassum H,Vishnoi S,Salman M,Raisuddin S,Parvez S

doi

10.1016/j.neulet.2016.02.001

subject

Has Abstract

pub_date

2016-03-23 00:00:00

pages

94-100

eissn

0304-3940

issn

1872-7972

pii

S0304-3940(16)30068-4

journal_volume

617

pub_type

杂志文章

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