International Journal of Clinical and Experimental Neurology
ISSN (Print): 2379-7789 ISSN (Online): 2379-7797 Website: https://www.sciepub.com/journal/ijcen Editor-in-chief: Zhiyou Cai, MD
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International Journal of Clinical and Experimental Neurology. 2015, 3(1), 21-25
DOI: 10.12691/ijcen-3-1-4
Open AccessArticle

Neuroprotective Role of Vitamin B3 in Experimentally Induced Oxidative Stress

Afaf El Atrash1, Lamees Dawood2, Ehab Tousson1, and Amira Salama1

1Zoology Department, Faculty of Science

2Medical Biochemistry, Faculty of Medicine, Tanta University, Tanta 31527, Egypt

Pub. Date: February 12, 2015

Cite this paper:
Afaf El Atrash, Lamees Dawood, Ehab Tousson and Amira Salama. Neuroprotective Role of Vitamin B3 in Experimentally Induced Oxidative Stress. International Journal of Clinical and Experimental Neurology. 2015; 3(1):21-25. doi: 10.12691/ijcen-3-1-4

Abstract

Paraquat is a widely used herbicide. The main mechanism underlying PQ toxicity is oxidative stress. Niacin (nicotinic acid) a precursor for NAD+ It has also been reported to possess oxygen radical scavenging activity. The enzyme PARP-1 is activated by DNA strand breaks, using NAD+ as a substrate. Thus, the present study aimed to assess the magnitude of oxidative DNA damage and the role of PARP and the advantages of modulating its activity by niacin supplementation in experimentally induced oxidative stress by PQ. 50 male albino rats were equally divided into five groups; the first and second groups were the control and PQ treated groups respectively while the 3rd group was nicotinic acid treated group; the 4th and 5th groups were co- and post treated PQ treated rats with nicotinic acid respectively. Serum 8-hydroxy-2'-deoxyguanosine and brain MDA levels in PQ treated group showed a significant increase when compared with control group, while levels of PARP activity and TAC in PQ treated group showed a significant decrease when compared with control group. A significant increase of PARP activity & TAC and a significant decrease in serum 8-hydroxy-2'-deoxyguanosine&MDA after nicotinic acid injection when compared with control group was observed. Post-treatment with nicotinic acid improved the biochemical and histopathological alterations in brain treated with nicotinic acid, while co-treatment with nicotinic acid protected against ROS production.

Keywords:
Paraquat Nicotinic acid Oxidative stress PARP-1 activity 8-OHdG MDA TAC

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