Effects of diazinon on the activity and gene expression of mitochondrial glutamate dehydrogenase from rat pancreatic Langerhans islets

The main propose of the present study was to determine the effects of diazinon on the activity and gene expression of glutamate dehydrogenase (GDH) as the key enzyme of Langerhans islet for secretion of insulin. Diazinon was administered intraperitoneally at doses of 15, 30, and 60 mg/kg. Langerhans islets were isolated from the pancreas of rats by a standard collagenase digestion, separation by centrifugation, and hand-picking technique. The activity and gene expression of the mitochondrial GDH was determined in the islets homogenates. Glutamate, C-peptide, and insulin were determined in plasma.Diazinon at all tested doses (15, 30, and 60 mg/kg) significantly (p < 0.01) decreased plasma insulin after 1 h while the values did not differ from control when examined after 18 h. Diazinon at all tested doses (15, 30, and 60 mg/kg) significantly (p < 0.01) increased concentration of C-peptide both 1 and 18 h post-administration. Diazinon at all tested doses (15, 30, and 60 mg/kg) significantly (p < 0.05) increased production of glutamate while the values did not differ from control when tested after 18 h. Administration of diazinon at doses of 30 and 60 mg/kg significantly (p < 0.001) increased activity of GDH after 1 h while all doses of diazinon increased GDH activity when measured after 18 h. Diazinon at dose of 60 mg/kg significantly (p < 0.01) decreased expression of GDH gene 18 h post-administration.It is concluded that GDH is a component of diazinon-induced changes in release of improper insulin.     

Biochemical evidence on positive effects of rolipram a phosphodiesterase-4 inhibitor in malathion-induced toxic stress in rat blood and brain mitochondria

Malathion is an organophosphate (OP) pesticide that has been shown to induce oxidative stress in brain through the generation of free radicals and alteration of the cellular antioxidant defense system independent of its anticholinesterase effects. The aim of this study was to investigate the possible protective role of rolipram as a selective phosphodiesterase (PDE) type 4 inhibitor, on toxicity of malathion, by measuring the activities of brain mitochondrial and plasma peroxynitrite (ONOO⁻), glutathione peroxidase (GPx), superoxide dismutase (SOD), Mn-SOD, catalase (CAT), and lipid peroxidation (LPO) in rats. Effective doses of malathion (200 mg/kg/day) and rolipram (200 μg/kg/day) were administered alone or in combination for 7 days by intraperitoneal injection. At the end of the experiment, the brain mitochondria and plasma of the animals were separated. In the brain cells mitochondria and blood plasma, the LPO, ONOO⁻, and GPx were higher in the malathion group as compared with controls. Rolipram ameliorated all of malathion-induced changes. Plasma CAT decreased in malathion-treated animals while it increased in brain mitochondria comparing with controls. Co-administration of rolipram with malathion improved CAT in both brain mitochondria and plasma. Malathion and rolipram did not alter total SOD or Mn-SOD in the plasma while both caused a significant elevation in brain mitochondria. In conclusion, this model of study that we employed, in a large extent, characterized the relationships among malathion-induced neurotoxicity, mitochondrial dysfunction, and significant increase in systemic and local oxidative/nitrosative stress in plasma and brain, respectively. Intracellular cAMP-elevating agents like rolipram, may be considered beneficial for the protection or recovery of malathion-induced toxic damage in brain mitochondria and blood.     

Stimulation of insulin and glucagon synthesis in rat Langerhans islets by malathion in vitro: Evidence for mitochondrial interaction and involvement of subcellular non-cholinergic mechanisms

We examined the effects of malathion, an organophosphorus (OP) insecticide, on glucagon, C-peptide, and insulin content or secretion from isolated rat Langerhans islets in vitro. Islets were isolated from the pancreas of rats by standard collagenase digestion, separation by centrifugation, and hand-picking technique. Then islets were cultured in medium and supplemented with various concentrations of malathion (25, 125, and 625 μg/ml) for 1, 3, and 5 h. In vitro exposure to malathion increased insulin and C-peptide contents at doses of 25, 125, and 625 μg/ml following 5 h incubation as compared to control. All doses of malathion increased glucagon content after 3 and 5 h as compared to control. Increase of the glucagon content at all doses in the fifth hour was higher than that of third hour. Malathion also decreased 2.8 and 16.7 mM glucose-stimulated insulin secretion at all doses after 30 min as compared to control.It is concluded that malathion reduce insulin exocytose in a short time (first hour) but after a long time (e.g., 5 h), the content of insulin is increased by compensating mechanisms such as resynthesize of insulin or aggregation of insulin. The present in vitro study for the first time proposes the involvement of subcellular non-cholinergic mechanisms in malathion-induced changes in Langerhans islets insulin and glucagon.     

Induction of insulin resistance by malathion: Evidence for disrupted islets cells metabolism and mitochondrial dysfunction

Hyperglycemia is observed with exposure to organophosphorus (OP) pesticides. The aim of this study was to investigate the effects of malathion on secretion of insulin from rat pancreatic islets in vitro and in vivo. Malathion was administered through food for 4 weeks at concentrations of 100, 200, and 400 ppm. For in vivo experiment, at the end of treatment, blood sample was obtained and plasma was separated. For in vitro experiment, the treated rats were anesthetized and underwent a laparatomy. The common bile duct was cannulated and the pancreas distended by injecting of cold collagenase V using peristaltic infusion pump. Islets were then hand picked under a stereomicroscope and cultured in the presence of various doses of glucose and KCl. Malathion at doses of 200 and 400 ppm increased plasma glucose and insulin concentrations and lowered activity of erythrocyte acetylcholinesterase. The isolated islets from pretreated animals with malathion 200 and 400 ppm showed lower glucose-stimulated insulin secretion while no change was observed in the presence of KCl. Light microscopic examination revealed that malathion causes patchy degenerative changes in pancreatic islets. Combination of in vivo and in vitro findings suggests that malathion induces a kind of insulin resistance that cannot overwhelm hyperglycemia. This action of malathion is mediated through disruption of islets mitochondrial function.     

Prophylactic effect of green tea polyphenols against liver and kidney injury induced by fenitrothion insecticide

The ameliorative effect of daily administrated dose of green tea extract (60 mg polyphenols/animal/day) was investigated on albino rats Rattus norvegicus (150-180 gm) intoxicated with 1/30 and 1/60 LD₅₀ fenitrothion organophosphate insecticide for 28 days. Blood samples were taken at 14 and 28 days for further biochemical parameters. Histopathological studies were carried out in the liver and kidney at the end of the experiment. Significant inhibition in plasma cholinesterase (ChE), a biomarker of Ops, was recorded. Damage in the liver and kidney tissues was observed and confirmed with elevation of plasma alanine aminotransferase (ALT), aspartate aminotaransferase (AST), albumin, urea and creatinine, as well as an elevation in the oxidative stress (OS) marker malondialdehyde (MDA). Decrease in total glutathione (GSH) content in erythrocytes and fluctuation in glutathione S-transferase (GST) activity in plasma was also observed. Green tea supplementation (60 mg/animal/day) partially counteracts the toxic effect of fenitrothion on oxidative stress parameters and repairs tissue damage in the liver and kidney, especially when supplemented to 1/60 LD₅₀ intoxicated animals depending on the duration. It seems that enzyme and metabolite markers of these organs need more time to be restored to the control level.     

Effects of diazinon on biochemical parameters of blood in rainbow trout (Oncorhynchus mykiss)

Existence of diazinon, an organophosphorous pesticide, in river waters of Iran near rice paddy fields has been reported by some authors. The present research aimed to determine the acute toxicity and evaluate the effect of sub-lethal concentrations of diazinon on some biochemical parameters of rainbow trout, Oncorhynchus mykiss after 7, 14 and 28 days. No significant differences were observed in the plasma levels of creatinine among the treatment groups at different sampling intervals. Acetylcholinesterase activity and the levels of total protein, albumin as well as globulin in plasma were significantly reduced at both concentrations tested (p < 0.05). Lactate dehydrogenase activity was only decreased on 7th day in 0.1 mg/L diazinon treatment (p < 0.05). Creatine kinase activity was significantly lower in 0.1 mg/L diazinon group at 14th and 28th sampling periods, whereas its activity significantly increased in fishes exposed to 0.2 mf/L diazinon only on 7th day (p < 0.05). Aspartate aminotransferase, alanine aminotransferase activities and glucose levels in diazinon treated groups were significantly higher than the controlled group at experimental periods (p < 0.05). In conclusion, long-term exposure to diazinon at sub-lethal concentrations induced biochemical alterations in rainbow trout, and offers a simply tool to evaluate toxicity-derived alterations.     

The effects of diazinon on pancreatic damage and ameliorating role of vitamin E and vitamin C

The aim of this study was to investigate effects of an organophosphate insecticide, diazinon (DI), on pancreas, and possible ameliorating role of vitamins E and C. We examined both in vivo and in vitro effects of DI on serum activities of alkaline phosphatase (ALP), γ-glutamyltransferase (GGT), amylase, and lipase enzymes. We also evaluated possible ameliorating effects of vitamins E and C combination against DI toxicity and blood levels of thiobarbituric acid reactive substances (TBARS) only in vivo. In vivo experimental groups were: control group, DI-treated group, and DI + vitamins E plus C-treated group. In vitro study groups were: control group and DI-treated group. The biochemical analyses were determined in in vitro experiments at both hour 0 and 24 while in in vivo experiments were determined only at hour 24. Lipase activity and TBARS level were found increased by DI in in vivo experiments while lipase activity was found decreased in in vitro experiments. Amylase and ALP activities were found decreased by DI in both in vivo and in vitro experiments. Also, the combination of vitamins E and C was found to partially improve these disorders. These results suggest that DI treatment causes pancreas damage via increasing oxidative stress in rats, and a combination vitamins E and C can reduce this lipoperoxidative effect.     

Biochemical and histopathological studies to assess chronic toxicity of triazophos in blood, liver and brain tissue of rats

Triazophos, O,O-diethyl-1-H-1,2,4-triazol-3-yl phosphorothioate, (TZ) is an organophosphorus pesticide which is extensively used in agriculture for controlling insect pests. Except a FAO/WHO report no study has investigated its short-term toxicity with respect to its potential to cause biochemical and histopathological alterations. The present study was designed to identify the effect of TZ at different doses (1.64, 3.2 and 8.2 mg/kg) on the oxidative stress parameters in blood as well as organs involved in xenobiotic metabolism (liver and brain) following chronic exposure for 90 days. Moreover, the study also delineates the effect of TZ on the histo-architecture of these organs. The results indicated a dose dependent induction (p < 0.001) of oxidative stress, as evident by increased malondialdehyde (MDA) level and compromised antioxidant defense including glutathione S transferase (GST) activity, glutathione (GSH) content and ferric reducing ability of plasma (FRAP) in blood, and increased MDA level with concomitantly decreased GSH content in tissues, following chronic exposure to TZ. The ratio of MDA: FRAP in blood was found to be increased following chronic exposure to TZ and may serve as a suitable indicator of severity of oxidative damage. Onset of such biochemical alterations is one of the early adaptive responses to TZ exposure which leads to histopathological alterations in terms of diffuse fatty changes expanding from mid-zonal area to whole lobule in liver. However, increased oxidative stress did not bring any morphological alteration in brain. The present study concludes that induction of oxidative stress, leading to subsequent histopathological alterations in liver, is an important mechanism underlying the TZ induced chronic toxicity.     

Effects of diazinon at different doses on rat liver and pancreas tissues

Diazinon is one of the most widely used organophosphates in agriculture. Toxic effects of diazinon are due to the inhibition of acetylcholinesterase, an enzyme needed for proper nervous system function. This study was designed to investigate the effects of diazinon at different doses on pancreas and liver tissues and in which dose level diazinon shows its effects. Sixty male Wistar albino rats were included in this study. Animals were initially divided into control and diazinon given groups. There were 10 animals in the control group and 50 animals in diazinon administered group. The latter was divided into five equal subgroups: 25, 50, 100, 200 and 300 mg/kg of diazinon administered groups. Control group was given only saline. All animals in 300 mg/kg diazinon group died. After 24 h, rats were sacrificed under ether anesthesia. Tissue and blood samples were taken for biochemical and histopathological analysis. Sample tissues were examined under light microscope. In biochemical analysis, AST, ALT, LDH, amylase and lipase enzyme activities were measured. One-way ANOVA test was used to compare the groups. In 200 mg/kg diazinon given group, it has been observed some histopathological changes in pancreas and liver tissues. Cholinesterase activities were significantly decreased and alkaline phosphatase levels were increased in all diazinon given groups, when compared with the controls. There was statistically significant difference between the control and diazinon given groups by means of serum amylase, lipase, ALT and AST activities (p < 0.05). LDH activities were significantly increased in 100 and 200 mg diazinon given groups, when compared with the controls (p < 0.05). Histopathological changes were observed only in 200 mg diazinon given group. This evidence suggest that diazinon effect is dose dependent and this is possibly 10-15% of the LD₅₀ dose (200 mg/kg), which cause acute pancreatitis and histopathological changes in liver.     

Tissue-specific antioxidative and neurotoxic responses to diazinon in Oreochromis niloticus

The purpose of this study was to evaluate oxidative stress and neurotoxic potential of organophosphorus (OP) insecticide diazinon in the sentinel freshwater fish, Oreochromis niloticus. Antioxidant and acetylcholinesterase (AChE) enzyme activities and malondialdehyde (MDA) and protein levels were measured spectrophotometrically in gill, kidney, alimentary tract, and muscle tissues of fish treated with sub-lethal diazinon concentrations for 1, 7, 15, and 30 days. Dose-dependent inhibitions of AChE were observed in all the experimental fish. On the contrary of alimentary tract, MDA levels were elevated in kidney and muscle and gill was not affected. AChE and MDA levels intercorrelated in kidney and muscle tissues. Diazinon had increased superoxide dismutase (SOD) activities in all the tissues, while kidney was the most affected tissue. Tissue-specific alterations were observed on catalase (CAT) and glutathione peroxidase (GPx) activities; however, the activities were not changed in gill and muscle tissues for GPx and in gill, muscle, and kidney tissues for CAT. Protein levels decreased in kidney, muscle, and alimentary tract, while increased in gill and alimentary tract in 15 days. With respect to these results, diazinon has oxidative and neurotoxic potentials in O. niloticus. Observed changes with diazinon treatment were generally tissue-specific and dose-dependent.     

A review on the mechanisms involved in hyperglycemia induced by organophosphorus pesticides

Organophosphorus (OP) compounds are cholinesterase-inhibiting chemicals used as pesticide. Exposures to OPs cause a significant number of poisonings and deaths each year. One of the reported adverse effects in human exposure to OPs is hyperglycemia. Animal studies have also shown altered glucose homeostasis following acute or chronic exposures to OPs. The objective of this paper is to provide a brief review of the mechanisms involved in the OP-induced glucose homeostasis alteration. To reach this objective, a search of the literature using Medline/Index Medicus, Scopus, and Chemical Abstract were performed, most of relevant citations were studied and summarized. To better understand the nature of glucose homeostasis, the principles of glucose production, metabolism, and its hormonal control have been discussed. Collection of theses studies support the conclusion that hyperglycemia is the outcome of acute or chronic exposure to OPs. OPs can influence body glucose homeostasis by several mechanisms including physiological stress, oxidative stress, inhibition of paraoxonase, nitrosative stress, pancreatitis, inhibition of cholinesterase, stimulation of adrenal gland, and disturbance in metabolism of liver tryptophan.     

Effects of atropine and pralidoxime pretreatment on serum and cardiac oxidative stress parameters in acute dichlorvos toxicity in rats

Recent several studies have reported that oxidative stress could be an important component of the mechanism of cardiotoxicity due to organophosphate-induced toxicity. The aim of this study is to evaluate the oxidative and antioxidative parameters in cardiac toxicity of organophosphate poisoning, and determine the effects of atropine and pralidoxime on this parameters. The experimental groups were randomly divided into five groups as control (corn oil), dichlorvos (30 mg/kg), atropine (10 mg/kg), pralidoxime (40 mg/kg), and atropine (10 mg/kg) + pralidoxime (40 mg/kg) groups. Serum cholinesterase levels were suppressed with dichlorvos, and these reductions were inhibited with atropine and/or pralidoxime pretreatment. Serum, but not cardiac, total free sulfhydryl groups and paraoxonase activities were significantly increased in the pralidoxime group when compared to the control group. Serum arylesterase activities were elevated in the dichlorvos, atropine, pralidoxime, and atropine + pralidoxime groups when compared to the control group (P < 0.05). Total oxidant status, oxidative stress index, malondialdehyde and catalase activities in serum and cardiac tissues were not markedly different between the groups. No significant changes were also observed with cardiac myeloperoxidase and serum ceruloplasmin activities. In conclusion, these results showed that acute dichlorvos administration did not cause marked cardiac damage, and oxidative stress probably does not play a major role in dichlorvos-induced poisoning. On the other hand, especially pralidoxime treatment markedly increased the serum total free sulfhydryl groups, paraoxonase and arylesterase activities. However, the underlying mechanisms for these changes are not exactly known.     

Protective effects of garlic (Allium sativum) extract upon lindane-induced oxidative stress and related damages in testes and brain of male rats

The purpose of this study, carried out on male Wistar rats, was to evaluate the beneficial effects of garlic (Allium sativum) extract injections upon lindane-induced damages in testes, brain and thyroid function. Under our experimental conditions, lindane poisoning (in drinking water for 30 days, supplying about 50 mg/kg body weight per day) resulted in a decreased weight of testes, epididymides, prostate gland and seminal vesicles (−52%, −42%, −50% and −5%, respectively), a decrease of spermatozoa count and motility (−56%, −37%, respectively), an increased level of free thyroxin (+84%) and decreased levels of TSH and FSH in serum (−74%, −77%, respectively). In addition, lindane treatment triggered an oxidative stress in testes and brain as revealed by an increased level of lipids peroxidation (TBARS) (+96%,+92%), an increase of superoxide-dismutase activity in testes (+69%) and a decrease of glutathione-peroxidase and catalase activities in testes and brain (−52%, −34% and −49%, −45%, respectively). These lindane-induced changes were almost reversed to normal in animals injected with a garlic extract (an amount corresponding to 300 mg fresh garlic/kg/day), what confirms a beneficial effect of this vegetal source of anti-oxidants.     

Monocrotophos induced lipid peroxidation and oxidative DNA damage in rat tissues

Monocrotophos (dimethyl(E)-1-methyl-2-(methyl carbamoyl) vinyl phosphate, MCP), a substituted vinyl phosphate, is a potent systemic toxicant and used for control of variety of pests. The present study is undertaken to evaluate the genotoxic potential of monocrotophos and time-dependent repair of the damaged DNA in rats, using single cell gel electrophoresis or comet assay. The involvement of oxidative stress was also examined by estimation of thiobarbituric acid reactive substances (TBARS) in the tissues of MCP exposed rats. The rats were given oral exposure of 4.5 and 9 mg MCP/kg body weight once as well as 0.3 and 0.6 mg MCP/kg body weight for 60 days. A dose-dependent increase was recorded in the levels of TBARS in the liver, kidney, spleen and brain of MCP exposed rats. Cytotoxicity of MCP is evident from the histopathological studies of rat tissues. The level of DNA damage was estimated by scoring 50 cells per animal, dividing into five types, Types 0, I, II, III and IV. The results clearly indicated that exposure to MCP, acutely or chronically, caused a dose-dependent increase in the number of damaged nuclei of Types II, III and IV in the liver, kidney, spleen and brain of rats. When the DNA damage was studied 48 and 72 h post MCP treatment, a significant reduction in the number of types III and IV nuclei was observed in all the tissues indicating a time-dependent repair. From the present study, it can be concluded that oxidative stress may be involved in the toxicity of MCP and MCP induces DNA damage in all the rat tissues exhibiting genotoxic potential in vivo.     

May antioxidants status depletion by Tetradifon induce secondary genotoxicity in female Wistar rats via oxidative stress?

Tetradifon is a potent organochlorine acaricide with an estrogen-like structure. The wide spread use of this chemical is likely to pollute the environment. Only few studies have been reported for the evaluation of its short- and long-term toxic effects including genotoxicity and carcinogenicity and there have been conflicting results in in vitro and in vivo test systems. In this work, we have evaluated Tetradifon for its ability to induce genotoxic damages in female Wistar rats. A single cumulative dose of 2430 mg/kg BW was administrated orally for 12 female rats of 190 g BW during 12 weeks. Twelve additional rats, no treated, have served as control. Animals were sacrificed after 6 and 12 weeks of treatment. Genetic toxicity studies were conducted in rats bone marrow, by chromosomal aberrations (CAs) and sister-chromatid exchanges (SCEs) assays. The oxidative stress status of treated animals has been also evaluated by assessment of lipid peroxidation by measuring thiobarbituric acid reactive substances (TBARS). Some serum parameters: vitamins (A and E), triglyceride (TG) and total antioxidants status (TAS) were determined. Our results showed a significant increase in tissue TBARS concentrations in the two treated groups suggesting that Tetradifon induce an oxidative stress. Elsewhere, rats treated with Tetradifon exhibited a statistical decrease in serum level of vitamin E and a significant depletion of serum total antioxidant status. Whereas, in comparison to control rats, treated animal cells did not show a significant increase in either the frequency of SCEs or CAs. These results indicate that Tetradifon did not present direct genotoxic effect in female Wistar rats. But we suggest that its inducting of an oxidative stress may lead to indirect mutagenecity that should be evaluated by other series of in vivo genotoxicity assays as micronucleus test or comet assay.     

Chlorpyrifos-induced oxidative stress and histological changes in retinas and kidney in rats: Protective role of ascorbic acid and alpha tocopherol

This study was undertaken to evaluate the antioxidant effect of vitamins C and E against oxidative stress, apoptosis and histological changes of kidney and retina in CPF-treated rats. Forty male Sprague-Dawley rats were divided into four groups including the control group, the group treated orally with a single dose of CPF (63 mg/kg b.w.), the group injected intramuscularly (i.m.) with vitamin C (250 mg/kg b.w.), and intraperitonealy (i.p.) with vitamin E (150 mg/kg b.w.) daily for 7 days and the group treated with CPF (single dose) and injected with vitamins (for 7 days). The results showed that CPF induced apoptosis and severe oxidative stress as indicated by the significant increase in MDA and sFasL concentration and the significant decrease in GSH concentration in serum. Co-administration of vitamins C and E ameliorate these toxic effects and improved the histological pictures of kidneys and retinas. It could be concluded that combined administration of vitamins C and E is useful in the routine therapy for the protection against tissue damage induced by CPF.     

Oxidative parameters of Rhamdia quelen in response to commercial herbicide containing clomazone and recovery pattern

In this study, fish Rhamdia quelen, were exposed to different concentrations of herbicide clomazone: 0.0 (control), 0.45 and 0.91 mg L⁻¹. After exposure for 8 days to herbicide, fish were transferred to clean water for a recovery period (8 days). Oxidative stress indicators such as thiobarbituric acid reactive substances (TBARS) levels and protein carbonyl content, as well as antioxidant defenses, such as catalase (CAT), superoxide dismutase (SOD), glutathione S-transferase (GST), ascorbic acid and non-protein thiols levels were studied, using the liver, brain and muscle tissues. Herbicide exposure increased TBARS in muscle and in liver at higher concentration. In liver protein carbonylation increased and catalase activity did not change in fish exposed to herbicide. SOD enhanced in liver at concentration of 0.91 mg L⁻¹. GST, ascorbic acid and non-protein thiols levels increase at both concentrations. At the end of the recovery period the most of the parameters recovered whereas GST and ascorbic acid remain elevated. The present study demonstrates the occurrence of disorders in antioxidant parameters and importance in the assessment of the potential risk of herbicides as clomazone on fish species.     

Single and simultaneous exposure of acetylcholinesterase to diazinon, chlorpyrifos and their photodegradation products

In vitro inhibition of electric eel acetylcholinesterase (AChE) by single and simultaneous exposure to organophosphorus insecticides diazinon and chlorpyrifos, and their transformation products, formed due to photoinduced degradation, was investigated. Increasing concentrations of diazinon, chlorpyrifos and their oxidation products, diazoxon and chlorpyrifos-oxon, inhibited AChE in a concentration-dependent manner. IC₅₀ (20 min) values, obtained from the inhibition curves, were (in mol/l): (5.1 ± 0.3) × 10⁻⁸, (4.3 ± 0.2) × 10⁻⁶ and (3.0 ± 0.1) × 10⁻⁸ for diazoxon, chlorpyrifos and chlorpyrifos-oxon, respectively, while maximal diazinon concentration was lower than its IC₅₀ (20 min). Calculated K_I values, in mol/l, of 7.9 × 10⁻⁷, 9.6 × 10⁻⁶ and 4.3 × 10⁻⁷ were obtained for diazoxon, chlorpyrifos and chlorpyrifos-oxon, respectively. However, 2-isopropyl-4-methyl-6-pyrimidinol (IMP) and 3,5,6-trichloro-2-pyridinol, diazinon and chlorpyrifos hydrolysis products, did not noticeably affect the enzyme activity at all investigated concentrations. Additive inhibition effect was achieved for lower concentrations of the inhibitors (diazinon/diazoxon ?1 × 10⁻⁴/1 × 10⁻⁸ mol/l i.e., chlorpyrifos/chlorpyrifos-oxon ?2 × 10⁻⁶/3 × 10⁻⁸ mol/l), while an antagonistic effect was obtained for all higher concentrations of the organophosphates. Inhibitory power of 1 × 10⁻⁴ mol/l diazinon irradiated samples can be attributed mostly to the formation of diazoxon, while the presence of non-inhibiting photodegradation product IMP did not affect diazinon and diazoxon inhibitory efficiencies.