Modulatory effects of vitamin C on biochemical and oxidative changes induced by acute exposure to diazinon in rat various tissues: Prophylactic and therapeutic roles

Abstract

Diazinon (DZN) as an organophosphate pesticide may cause oxidative stress in different tissues. Antioxidants increase tissue protection from oxidative stress. The aim of the present study was to investigate prophylactic and therapeutic effects of vitamin C against oxidative stress caused by DZN in various tissues of male Wistar rats. Thirty rats were divided into five groups: control group received corn oil as DZN solvent, DZN group received 100 mg/kg of DZN, C group received 200 mg/kg of vitamin C, C‐DZN and DZN‐C groups received vitamin C before and after DZN injection. Plasma and various tissues were prepared and evaluated for measurement of the biochemical parameters and oxidative stress biomarkers. Results showed that acute administration of DZN significantly increased superoxide dismutase and glutathione‐S‐transferase activities and malondialdehyde level in all tissues, catalase (CAT) activity in liver, kidney and heart and some plasma biochemical indices, while it decreased cholinesterase and lactate dehydrogenase activities and glutathione content in all tissues. CAT activity in erythrocytes, brain and spleen was decreased in DZN‐exposed rats compared with the control group. Administration of vitamins C in both prophylactic and therapeutic groups ameliorated in these parameters, although all these tests in tissues did not return to the normal level. These data suggest that oxidative stress is an essential mechanism involved in DZN‐induced adversity effect, as evidenced by the altered activity of antioxidant enzymes, depleted GSH content and the enhanced membrane lipid peroxidation. Both the prophylactic and therapeutic treatments of rats to vitamin C have beneficial effects against oxidative stress and cholinergic hyperactivity induced by DZN in tissues especially in the brain tissue through free radical scavenging.

Tissues toxicity attenuation by vitamin E on oxidative damage induced by diazinon

“…Similarly, ROS produced from the metabolism of DZN may damage other tissues such as heart, kidney and spleen causing the leakage of enzymes from the tissues into plasma [21]. However, the reduced these parameters levels in groups pre-and post-treated with vitamin E showed that the antioxidant vitamin E protected the tissues from the lipoperoxidative changes provoked by DZN, probably due to its free radical scavenging ability [2,25]. Damodar et al [26] have reported that co-administration of vitamin E with DZN to rats resulted in insignificant improvement of the liver enzyme activities.…”

“…The elevated these enzymes activities in DZN exposed rat may be due to leakage from the liver and heart tissues as a result of DZN-induced lipid peroxidation of membrane [24]. In addition, significant increases of plasma creatinine, urea and uric acid levels may due to the impairment of the glomerular function and tubular damage in the kidneys caused by DZN through induction of oxidative stress [2,5]. Similarly, ROS produced from the metabolism of DZN may damage other tissues such as heart, kidney and spleen causing the leakage of enzymes from the tissues into plasma [21].…”

“…These compounds inhibit acetylcholine-esterase (AChE) enzyme activity, which causes the accumulation of acetylcholine (ACh) in the synaptic cleft that causes hypercholinergic symptoms. Poisoning by OPs is one of the global health problems and are responsible for the third most common cause of poisoning in Iran [1][2][3]. Diazinon (DZN) is one of the most important OP insecticides that is used extensively for various health-related and agricultural purposes pesticides in Iran [4].…”

“…DZN causes some hematological, biochemical and histological alterations in rat, rabbits and mice. Its exposure may also cause alterations many systems such as the immune system, urinary system, reproductive system, pancreas and liver [2,6]. Furthermore, DZN produces oxidative stress through the formation of reactive oxygen species (ROS) and alterations in antioxidants status in mammals and other organisms [2,7,8].…”

Sodium benzoate induces neurobehavioral deficits and brain oxido‐inflammatory stress in male Wistar rats: Ameliorative role of ascorbic acid

“…[ 5 ] Although some studies have reported that SB‐treated rats showed anxiogenic behaviors and alteration in rats' cerebellar structure, [ 18,34 ] AA has been reported to have neuroprotective effects against neurotoxicity in rats. [ 33,35 ] There is contrasting information on the effect of Coadministration of SB and AA in vivo. Kehinde et al showed that AA coadministered with SB aggravated damage to male Wistar rats' testicular function.…”