PCB (Aroclor 1254) enhances oxidative damage in rat brain regions: protective role of ascorbic acid.
PCBs are one of the environmental toxicants and neurotoxic compounds which induce the production of free radicals leading to oxidative stress. Oxidative stress is a contributing factor to alteration caused in neurodegenerative processes. The ability of Vitamin C to retard oxidative processes has been recognized for many years. Therefore, the present experiment was carried out to determine the antioxidant role of ascorbate on Aroclor 1254 induced oxidative stress in brain regions of albino rats. One group of rats received corn oil as vehicle for 30 days as control. The other group of rats were administered Aroclor 1254 at a dose of 2 mg/kg bw/day intraperitoneally for 30 days. One group of rats received Vitamin C (100 mg/kg bw/day) orally simultaneously with Aroclor 1254 for 30 days. The brain was dissected to cerebral cortex (Cc), cerebellum (C) and hippocampus (H). Enzymatic and non-enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), reduced glutathione (GSH) and Vitamin C were estimated. Hydrogen peroxide (H(2)O(2)), lipid peroxidation (LPO) and acetylcholine esterase activity (AchE) were determined. Activities of SOD, CAT, GPx, GST, AchE and the concentration of GSH, Vitamin C were decreased while an increase in H(2)O(2) and LPO were observed in brain regions of PCB treated animals. Vitamin C administration retrieved all the parameters except GST, significantly. These results suggest that PCB induces oxidative stress in rat brain by decreasing the activities of antioxidant enzymes, which can be protected by Vitamin C treatment.
Venkataraman
Prabhu
P
Department of Endocrinology, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani, Chennai 600113, India.
Muthuvel
Raju
R
Krishnamoorthy
Gunasekaran
G
Arunkumar
Arumugam
A
Sridhar
Muthusami
M
Srinivasan
Narasimhan
N
Balasubramanian
Karundevi
K
Aruldhas
Maria Michael
MM
Arunakaran
Jagadeesan
J
D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000627:therapeutic use*; D001205:Ascorbic Acid / Q000378:metabolism / Q000627:therapeutic use*; D001835:Body Weight / Q000187:drug effects; D001921:Brain / Q000473:pathology*; D002374:Catalase / Q000378:metabolism; D020111:Chlorodiphenyl (54% Chlorine) / Q000037:antagonists & inhibitors* / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D050356:Lipid Metabolism / Q000187:drug effects; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009929:Organ Size / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism
D000975:Antioxidants; D017382:Reactive Oxygen Species; D020111:Chlorodiphenyl (54% Chlorine); D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005982:Glutathione Transferase; D000110:Acetylcholinesterase; D005978:Glutathione; D001205:Ascorbic Acid