Diazinon-induced brain toxicity and protection by vitamins E plus C

Abstract

Diazinon (DI) is a widely used pesticide in agriculture, resulting in environmental deleterious effects on neural systems. The current study was performed to investigate the effects of treatment with vitamins E plus C on brain toxicity, which is possibly induced by DI. Twenty-one male rats were divided into three groups (n = 7/group) as follows: (1) control group (C); (2) DI-treated group (DI); (3) DI + vitamins E plus C-treated group (DI + Vit). In order to examine lipid peroxidation and antioxidant status in rats, the level of malondialdehyde (MDA), activities of two free radical scavanging enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) have been studied in brain of rat. The results showed that treatment with DI induced significant (p < 0.05) increases in the level of serum MDA in rat brain. The vitamins E plus C combination reduced lipid peroxidation in rat brain. The activity of SOD level was significantly higher in DI + Vit group, compared to the control group. GSH-Px, SOD and CAT values were not significantly different in the DI group than in control. Oxidative stress contributes to DI-induced brain toxicity. Our results suggested that vitamins E plus C combination may have a protective effect on DI-induced brain toxicity.

Strain-Related Differences on Response of Liver and Kidney Antioxidant Defense System in Two Rat Strains Following Diazinon Exposure

“…These findings are in agreement with the results of the previous reports that showed SOD and CAT activities were increased in fish liver [22] and rat heart and brain after exposure to DZN [11]. Other studies have also showed that DZN increased SOD activity no change in CAT activity in rat brain [23] and in fish gill, kidney and muscle [24]. Our result is in contrast with the findings of Shah and Iqbal [4] that showed treatment of rats with DZN orally (10 -30 mg/kg daily for 8 weeks) decreases the activities of renal antioxidant enzymes.…”

“…The enhanced lipid peroxidation shows that DZN-induced ROS are not totally scavenged by the antioxidant enzymes. These findings are in agreement with the results of other studies that showed oral administration of DZN caused increase of MDA level in kidney, brain, heart and muscle of rat [4,11,23].…”

Influence of Sibinin on DMBA Induced Hepatotoxicity and Free-Radical Damage in Norwegian Rat, Rattus norvegicus (L).

“…ve Tic. AS, Izmir, Turkey)with corn oil (Shah and Iqbal, 2010;Yilmaz et al, 2012 andTeimouri, 2007); -Group 3: Silibinin group (n = 8); silibinin was given orally, 100 mg/kg/day every 24 hours, for 7 days (Arthur, 2000 andNakagawa andMoore, 1999); -Group 4: DMBA + Silibinin group (n = 8); rats were given DMBAsingle dose of 335 mg/kg BW of DMBA orally and 100 mg/kg/ day silibinin was administered orally, every 24 hours for 7 days.…”

Dose-Response and Time-Course of a-Tocoferol Mediating the Cytoprotection Of Dental Pulp Cells Against Hydrogen Peroxide

“…Previous studies have demonstrated α-T efficacy against HP-induced oxidative stress on different cell types, such as astrocytes, placental cells, fibroblasts and hepatocytes (13,14). Additionally, α-T increases the expression of endogenous antioxidants, such as dismutase superoxide and catalase (15)(16)(17), and reduces gene expression of inflammatory mediators (9). In this way, α-T has an effective role in antioxidant and antiinflammatory events (24).…”

“…Nevertheless, it is known that the antioxidant action of VE is mediated by its alpha-tocopherol (α-T) isomer, which has the capacity to incorporate to the cell membrane and stop lipid peroxidation propagation (11). Several researchers have assessed the protective effect of α-T and confirmed its capacity to prevent oxidative stress propagation, stabilize the cell membrane, enhance cell viability and increase the amount of endogenous antioxidants (12)(13)(14)(15)(16)(17).…”