title: 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.
authors: Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), New Delhi 110062, India.
authors: Mohammad
authors: M
authors: Ashafaq
authors: Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), New Delhi 110062, India.
authors: Heena
authors: H
authors: Tabassum
authors: Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), New Delhi 110062, India.
authors: Shruti
authors: S
authors: Vishnoi
authors: Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), New Delhi 110062, India.
authors: Mohd
authors: M
authors: Salman
authors: Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), New Delhi 110062, India.
authors: Sheikh
authors: S
authors: Raisuddin
authors: Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), New Delhi 110062, India. Electronic address: drsuhelparvez@yahoo.com.
authors: Suhel
authors: S
authors: Parvez
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001522:Behavior, Animal / Q000187:drug effects; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D004785:Environmental Pollutants / Q000633:toxicity*; D016166:Free Radical Scavengers / Q000494:pharmacology; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009942:Organometallic Compounds / Q000633:toxicity*; D018384:Oxidative Stress / Q000187:drug effects; D017208:Rats, Wistar; D013634:Tannins / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D004785:Environmental Pollutants; D016166:Free Radical Scavengers; D009942:Organometallic Compounds; D013634:Tannins; C008261:lead acetate
keywords: Antioxidant; Biomarker; Brain; Lipid peroxidation; Oxidative stress