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Nonsteroidal anti-inflammatory drugs are associated with an increase in cardiovascular events despite its uses in the therapeutic agent for the management of long- and short-term pain. Over the last years, evidence has accumulated showing that oxidative stress plays an important role in the pathogenesis of cardiovascular diseases. Oxidative stress is no longer considered as a simple imbalance between the production and scavenging of reactive oxygen species (ROS), but as a dysfunction of enzymes involved in ROS production. This study investigated the effect of diclofenac on the activity of oxidative stress enzymes as well as formation of lipid peroxidation. Male rats weighing about 100-120 g were divided into four groups: group one (control, feed+water) group two, group three and group four treated with different mg/kg/day of drugs (50 mg/kg/day, 100 mg/kg/day and 150 mg/kg/day) feed and water respectively for 7 days. Analysis on the effect of diclofenac on the activities of stress enzymes such as nicotine adenosine dinucleotide phosphate hydrogenase oxidase (NADPHoxidase), xanthine oxidase(XOD), catalase(CAT), superoxide dismutase(SOD) and Glutathione Peroxidase as well as evaluation of lipid peroxidation by measuring malondialdehyde (MDA) in the heart homogenate were carried out and the result showed a significant increase in each parameter given rise to the production of reactive oxygen species (ROS) if not moderated by the antioxidant defense can lead to cardiac impairment as a result of oxidative stress damage or injury. The result obtained implies that diclofenac (NSAIDs) affects the redox status of vascular tissues (heart tissues).
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