This study is aimed at analysing biochemical and genetic endpoints of toxic effects after administration of adrenaline. For this purpose, the study was carried out on Wistar rats and three doses of adrenaline were used: 0.75 mg/kg, 1.5 mg/kg, and 3 mg/kg body weight. To achieve these aims, we investigated the effects of adrenaline on catalase (CAT), Cu, Zn-superoxide dismutase (SOD), malondialdehyde (MDA), nitrite (NO2−), carbonyl groups (PCC), and nitrotyrosine (3-NT). Total activity of lactate dehydrogenase (LDH), its relative distribution (LDH1–LDH5) activity, level of acute phase proteins (APPs), and genotoxic effect were also evaluated. The obtained results revealed that all doses of adrenaline induced a significant rise in CAT activity, MDA level, PCC, NO2−, and 3-NT and a significant decrease in SOD activity compared to control. Adrenaline exerted an increase in total activity of LDH, LDH1, and LDH2 isoenzymes. Further study showed that adrenaline significantly decreased serum albumin level and albumin-globulin ratio, while the level of APPs (α1-acid glycoprotein and haptoglobulin) is increased. The micronucleus test revealed a genotoxic effect of adrenaline at higher concentrations (1.5 mg/kg and 3 mg/kg body weight) compared to untreated rats. It can be concluded that adrenaline exerts oxidative and nitrative stress in rats, increased damage to lipids and proteins, and damage of cardiomyocytes and cytogenetic damage. Obtained results may contribute to better understanding of the toxicity of adrenaline with aims to preventing its harmful effects.

Chlorpyrifos is a widely used organophosphate pesticide (OP). In birds and mammals OP exhibits a toxic effect via inhibition of cholinesterases [acetylcholinesterase (AChE) and butyrylcholinesterase (BChE)] and through oxidative/nitrosative stress. In this study, the influence of chlorpyrifos on cholinesterase activity, parameters of oxidative stress [malondialdehyde (MDA); glutathione (GSH); superoxide dismutase (SOD); nitrite concentration (NO2-); hydrogen peroxide (H2O2)], and inflammatory parameter [activity of myeloperoxidase (MPO)] in the brain of Japanese quail (Coturnix japanica) was examined. The study was conducted on a total of 60 male Japanese quails (one control and 5 experimental groups, n = 10), 3 to 4 wk old. Quails were administered by gavage chlorpyrifos (CPF) for 7 consecutive da at doses of 0.375 mg/kg BW, 0.75 mg/kg BW, 1.5 mg/kg BW, 3 mg/kg BW, and 6 mg/kg BW. Our studies have shown that all doses of CPF significantly inhibited both cholinesterases in brain: AChE from 22.74 to 37.83% and BChE from 19.53 to 61.9%, and that inhibition was dose dependent. Also, CPF has led to an increase in the concentration of MDA, GSH, NO2-, and H2O2 and activity of SOD and MPO. Overall, these results support the hypothesis that CPF causes oxidative stress and inflammatory response. This research was carried out on quails because there is hardly any or not enough data about the neurotoxic effect of CPF and especially about its influence on oxidative stress in birds. This study is highly important because we are witnessing massive avian mortality in certain countries due to pesticides.

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Inhibition of acethylcholinesterase (AChE) as a key molecular event induced by organophosphate (OP) pesticides and nerve agents presents a human health concern. In efficacy testing of experimental oximes, potential antidotes in OP poisoning, reactivation of OP-inhibited AChE is used as specific endpoint. However, according to our best knowledge, so far oximes have not been quantitatively evaluated by comprehensive benchmark dose (BMD) approach, that would improve both identification and quantification of the effect and allow more rigorous comparison of efficacies. Thus, we have examined in vivo dose-response relationship for two promising experimental oximes, K203 and K027, concerning reactivation of erythrocyte AChE inhibited by dichlorvos (DDVP). Groups of Wistar rats were treated with six different doses of oximes (i.m) immediately after DDVP challenge (s.c) and AChE was measured 60 min later. Dose-response modeling was done by PROAST software 65.5 (RIVM, The Nederlands). BMD-covariate method resulted in four-parameter model from both exponential and Hill model families as the best estimate of relationship between AChE activity and oxime dose, with potency parameter being oxime-dependent. Oxime K027 was shown to be 1.929-fold more potent considering that 58% increase in AChE activity was achived with the dose BMD-K027 = 52 μmol/kg in contrast to BMD-K203 = 100 μmol/kg.

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