Afaf El Atrash¹, Lamees Dawood², Ehab Tousson^1,, Amira Salama¹

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.

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