Effects of diazinon on antioxidant defense system and lipid peroxidation in the liver of Cyprinus carpio (L.)

Abstract

Diazinon is a widely used organophosphorus pesticide in agriculture and environmental health, hence its adverse effects on nontarget animals, especially on fish is to be determined. The present study therefore aimed at detecting the biochemical changes caused by diazinon. To accomplish this aim, we studied the effects of sublethal concentrations (0.0036, 0.018, and 0.036 ppb) of diazinon on acetylcholine esterase activity, antioxidant enzyme activities, and lipid peroxidation in the liver of Cyprinus carpio on days 5, 15, and 30 after the exposure. The results revealed that the antioxidant enzyme activities such as superoxide dismutase, glutathione peroxidase, and catalase were induced by diazinon exposure. In addition, the highest catalytic activity of glutathione S-transferase (GST) was obtained with 1-chloro-2, 4-dinitrobenzene (CDNB). GST activity toward 1,2-dichloro-4-nitrobenzene (DCNB) was also observed in the liver, yet it was relatively low as opposed to the other substrates tested. On the other hand, hepatic malondialdehyde level did not show any significant alteration except after the exposure on day 15. The exposure of low concentrations of diazinon to C. carpio can induce oxidative stress in liver; yet restoring susceptibility and adapting to oxidative stress are likely to occur when low level of oxidative stress is administered. Furthermore, no significant change was observed in hepatic lipid peroxidation after diazinon treatment indicating that liver tissue resisted to oxidative stress by enhancing their antioxidant mechanisms. The level of lipid peroxidation was assumed to be associated with the concentrations of diazinon and experimentation periods. The induction of glutathione S-transferase and antioxidant enzyme activities were also assumed to have resulted from the defense against the toxicity of diazinon.

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

“…The increased of these enzyme activities are probably a response to neutralize the impact of increased ROS generation in tissues. 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].…”

“…Elevated GST activity may reflect the possibility of better protection against pesticide toxicity [1,11]. The increased GST activity following exposure to DZN in various tissues of fish has been reported previously [11,13,22]. In addition, GST activity was not significantly affected after exposure to some OPs [21,26].…”

Toxicological and physiological effects of ethephon on the model organism, Galleria mellonella L. 1758 (Lepidoptera: Pyralidae)

“…In that study, the author reported that GST activity in hemolymph of G. mellonella larvae increased at low doses of GA 3 treatment. Similar results have also been reported with GST activity by organophosphate insecticides and other PGRs in vertebrate animals and insects (Yu, 2004;Hyrsl et al, 2007;Oruc, 2011;Tuluce & Çelik, 2006). We assume that GST activity can be used as a biomarker to evaluate ecotoxicological properties of ETF for insects.…”

“…On the other hand, the MDA level decreased to control level again at higher doses of ETF after 48 h. In addition, a considerable decrease was recorded between 24 and 48 h at 330 and 360 µg/5 µl. This decrease may be associated with the increasing activity of GST with time and ETF doses (Figure 2), because, GST, a phase II detoxifying enzyme, has an important role in the cellular detoxification of stressors in insects (Hyrsl et al, 2007;Oruc, 2011;Erdem & Büyükgüzel, 2015;Altuntaş, 2015a). Therefore, the increase in GST activity may be related to an inhibition of the lipid peroxidation process and physiological response mechanism against ETF toxicity for cellular detoxification.…”

Adverse effects of organophosphorus pesticides on the liver: a brief summary of four decades of research

“…Extensive data suggest that free radical formation and oxidative stress can be a major contributor to the toxicity of pesticides (108)(109)(110)(111)(112)(113). OPs are oxidants and impair enzymatic antioxidant defences, including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione S-transferase (GST) (23,34,44,(114)(115)(116)(117)(118)(119)(120)(121)(122)(123)(124)(125)(126)(127)(128)(129). Malathion, methyl parathion, and parathion in HepG2 cell lines, as well as chlorpyrifos, methidathion, chlorfenvinphos, and dimethoate in rat liver and diazinon in fish most probably disrupt membrane lipids through oxidative stress (23,35,61,116,118,(130)(131)(132)(133)(134)(135).…”