Impact of continuous Triazophos exposure on Labeo rohita: Physiological, biochemical, and histological alterations and IBRv2 index assessment.

Pesticides are commonly used in agriculture and aquaculture. Triazophos, an organophosphate-based pesticide, is widely used in agriculture to control many insect pests. Due to its high photochemical stability and mode of action, Triazophos could persist in the aquatic ecosystem and cause toxic effects on non-target organisms. We have studied the potential toxic effects of Triazophos on L. rohita. Primarily, we determined the median lethal concentration (LC50) of Triazophos for 24 and 96 h. Next, we studied acute (96 h, LC50-96 h) toxicity. Then, we studied chronic (35 days, 1/10th LC50-24 h Treatment I: 0.609 mg/L, 1/5th LC50-96 h Treatment II: 1.044 mg/L) toxicity. We analyzed blood biomarkers such as hematology (Hb, Hct, RBC, WBC, MCV, MCH and MCHC), prolactin, cortisol, glucose and protein levels. Concurrently, we analyzed tissue biomarkers such as glycogen, GOT, GPT, LDH and histopathology. IBRv2 index assessment method was also to evaluate the Triazophos toxicity. Studied hematological, hormonal, biochemical and enzymological biomarkers were affected in Triazophos treated groups when compare to the control group. The changes in these biomarkers were statistically significant at the 0.05 alpha level. Triazophos exposed fish shown a severe degenerated primary and secondary lamellae, lamellar fusion, hypertrophy and telangiectasia in the gills. In the hepatic tissue, it caused moderate necrosis, blood congestion, distended sinusoids with minor vacuolation, prominent pyknotic nuclei, hypertrophy, cloudy swelling of cells, lipid accumulation and fibrotic lesions. In the renal tissue, Triazophos caused thickening of Bowman's capsule, hyaline droplets degeneration, irregular renal corpuscle, congestion, cellular swelling, degeneration of tubular epithelium, necrosis, shrunken glomerulus, vacuolated glomerulus, hypertrophy, exudate and edema. IBRv2 analysis suggested that tissue biomarkers are highly sensitive to Triazophos toxicity and prolonged exposure could cause serious health effects like acute toxicity in fish. Triazophos could cause multiorgan toxicity at studied concentrations.

Comprehensive multi-omics investigation of sub-chronic toxicity induced by Cadmium and Triazophos Co-exposure in hook snout carps (Opsariichthys bidens).

The coexistence of heavy metals and pesticides poses a critical challenge in agricultural ecosystems. Traditional toxicity assessments often focus only on the individual impacts of either pesticides or heavy metals. Here, the untargeted metabolomics and 16 S rRNA sequencing were used to assess the individual and combined effects of cadmium (Cd) and triazophos (TRI) on hook snout carps (Opsariichthys bidens). Cd caused much more serious impacts on hepatic metabolism and gut microbiota than those in TRI. Combined Cd and TRI exposure synergistically affected hepatic metabolism, causing mitochondrial dysfunction and even oxidative damage. Simultaneously, 16 S rRNA sequencing highlighted significant variations in the composition and abundance of gut microbiota. A noteworthy connection emerged between these distinct microbiota profiles and disruptions in energy metabolism, ultimately leading to disorders in metabolites. These findings enhanced the understanding of risks posed by heavy metals and pesticides, providing insights for better environmental risk assessments of aquatic organisms.

Synergistic risk in the gut and liver: Insights into the toxic mechanisms and molecular interactions of combined exposure to triazophos and fenvalerate in zebrafish.

The simultaneous or sequential application of pesticides such as triazophos (TRI) and fenvalerate (FEN) in agriculture results in their residues co-existing in the environments. However, the impact of co-exposure to TRI and FEN on the gut-liver axis, along with the underlying mechanisms, remains unclear. Our results showed that exposure to FEN (96 h-LC50 value of 0.096 mg a.i. L-1) was more toxic to adult zebrafish compared to TRI (96 h-LC50 value of 6.75 mg a.i. L-1). Furthermore, the study aimed to reveal the toxic potencies of individual and combined exposure to TRI and FEN on the liver-gut axis in zebrafish (Danio rerio). Our results also indicated that pesticide exposure decreased tight junction molecule expression and increased intestinal inflammatory molecule expression in D. rerio, with co-exposure demonstrating enhanced toxicity. Co-exposure altered gut flora structure and species abundance. RNA-Seq sequencing revealed changes in liver gene expressions, particularly enrichment of P53 signaling. Molecular docking demonstrated FEN's stronger binding to P53 and Caspase3, correlating with its higher toxicity. Liver pathology confirmed exacerbated liver damage by individual and co-exposures, with co-exposure inducing more severe liver injury. qPCR results showed increased pro-apoptotic gene expression and decreased anti-apoptotic gene expression, with co-exposure exhibiting an interactive effect. Overall, this study identifies specific targets and pathways influenced by these pesticides, revealing toxicity mechanisms involving the gut-liver axis, which is crucial for environmental risk assessment of pesticide mixtures.

Combined Transcriptomics and Metabolomics Analysis Reveals Profenofos-Induced Invisible Injury in Pakchoi (Brassica rapa L.) through Inhibition of Carotenoid Accumulation.

Profenofos insecticide poses risks to nontarget organisms including mammals and hydrobionts, and its effects on crops are not known. This study examined the invisible toxicity of profenofos on pakchoi (Brassica rapa L.), using transcriptome and metabolome analyses. Profenofos inhibited the photosynthetic efficiency and light energy absorption by leaves and severely damaged the chloroplasts, causing the accumulation of reactive oxygen species (ROS). Metabolomic analysis confirmed that profenofos promoted the conversion of ß-carotene into abscisic acid (ABA), as evidenced by the upregulation of the carotenoid biosynthesis pathway genes: zeaxanthin epoxidase (ZEP), 9-cis-epoxycarotenoid dioxygenase (NCED3), and xanthoxin dehydrogenase (XanDH). The inhibitory effects on carotenoid accumulation, photosynthesis, and increased ABA and ROS contents of the leaves led to invisible injury and stunted growth of the pakchoi plants. The findings of this study revealed the toxicological risk of profenofos to nontarget crops and provide guidance for the safe use of insecticides.

Co-exposure to cadmium and triazophos induces variations at enzymatic and transcriptional levels in Opsariichthys bidens.

Heavy metals and pesticides are significant pollutants in aquatic environments, often leading to combined pollution and exerting toxic effects on aquatic organisms. With the rapid growth of modern industry and agriculture, heavy metal cadmium (Cd) and pesticide triazophos (TRI) are frequently detected together in various water bodies, particularly in agricultural watersheds. However, the combined toxic mechanisms of these pollutants on fish remain poorly understood. This experiment involved a 21-day co-exposure of Cd and TRI to the hook snout carp Opsariichthys bidens to investigate the toxic effects on liver tissues at both enzymatic and transcriptional levels. Biochemical analysis revealed that both individual and combined exposures significantly increased the content or activity of caspase-3 (CASP-3) and malondialdehyde (MDA). Moreover, the impact on these parameters was greater in the combined exposure groups compared to the corresponding individual exposure groups. These findings suggested that both individual and combined exposures could induce mitochondrial dysfunction and lipid peroxidation damage, with combined exposure exacerbating the toxicological effects of each individual pollutant. Furthermore, at the molecular level, both individual and combined exposures upregulated the expression levels of cu-sod, cat, and erß, while downregulating the expression of il-1. Similar to the patterns observed in the biochemical parameters, the combined exposure group exhibited a greater impact on the expression of these genes compared to the individual exposure groups. These results indicated that exposure to Cd, TRI, and their combination induced oxidative stress, endocrine disruption, and immunosuppression in fish livers, with more severe effects observed in the combined exposure group. Overall, the interaction between Cd and TRI appeared to be synergistic, shedding light on the toxic mechanisms by which fish livers responded to these pollutants. These findings contributed to the understanding of mixture risk assessment of pollutants and were valuable for the conservation of aquatic resources.

Sex-specific metabolic dysregulation in digestive glands of green mussels following exposure to triazophos.

As a ubiquitous environmental pollutant in China, triazophos (TP) is known to have neurotoxicity, oxidative stress, and reproductive toxicity to mussels. To investigate the molecular mechanisms of TP toxicity, metabolic changes in the digestive glands of Perna viridis in different sexes were examined after treated with 35 µg/L TP. Notably, 158 significant different metabolites (SDMs) were detected in TP-treated mussels and more than half of the SDMs were lipids and lipid-like molecules, which suggested that TP disturbed the lipid metabolism of P. viridis. In addition, metabolites associated with neurotoxicity and reproductive disturbance were also detected in female and male mussels. Moreover, a larger number of SDMs were found in male mussels (120 SDMs) than females (99 SDMs), and 60 common metabolites exhibited consistent variation tendency and similar magnitude in both sexes. The metabolic alternations in female and male mussels displayed similar protective mechanisms and also sex-specific responses, male mussels were more sensitive to TP exposure. This research provided new data about the molecular mechanisms of TP toxicity and the gender specific changes in mussels after treated by chemicals.

Triazophos-induced Respiratory and Behavioral Effects and Development of Adverse Outcome Pathway (AOP) for short-term Exposed Freshwater Snail, Bellamya Bengalensis.

The physiological effects of triazophos were examined using respiratory and behavioral endpoints in Bellamya bengalensis under a 96-hour acute exposure regime. Physiological manifestation of respiratory stress was measured using the rate of oxygen consumption while behavioral toxicity was measured using crawling reflexes, touch response, and mucus production. The threshold effect values for LOEC (Lowest Observed Effect Concentration), NOEC (No Observed Effect Concentration), and MATC (Maximum Acceptable Toxicant Concentration) at 96 h were 0.40, 0.60, and 0.075 mg/l, respectively. Definitive 96 h acute exposures for both respiratory and behavioral endpoints tests were determined using a control group and concentrations ranging from 0.40 to 1.60 mg/l monitored for 24, 48, 72, and 96 h. Test organisms irrespective of exposure concentration demonstrated an initial rise in oxygen consumption rate after 24 h, followed by a progressive decrease in toxicant concentration and exposure period. The in silico structural analysis presents triazophos as having an electrophilic toxic structure similar to choline esterase inhibitors, and also capable of inducing oxidative stress. The AOP highlighted neurotoxicity and oxidative stress as plausible pathways of triazophos toxicity in mollusk species.

The interactive effect of anti-sea lice pesticide azamethiphos and temperature on the physiological performance of the filter-feeding bivalve Ostrea chilensis: A non-target species.

The pesticide azamethiphos used by the salmon industry to treat sea lice, is applied as a bath and subsequently discharged into the sea. The effects of azamethiphos concentration (0, 15 and 100 µg L-1) on the physiology of the Chilean oyster (Ostrea chilensis) at two temperatures (12 and 15 °C) was examined. In all azamethiphos treatments, oysters kept at 15 °C had clearance rates (CR) higher than oysters kept at 12 °C. The oxygen consumption rate (OCR) increased at higher temperatures, except with 100 µg L-1 of azamethiphos, where no changes were observed. Sixty days after the exposure, survival rates of 91 and 79% (15 and 100 µg L-1, respectively), were observed compared to the controls, a situation independent of the experimental temperature. The interaction between temperature and pesticide has detrimental effects on the physiological performance and survival of O. chilensis, and these effects should also be assessed for other non-target species.

Evaluation of the acute toxic response induced by triazophos to the non-target green algae Chlorella pyrenoidosa.

Residues of triazophos in aquatic ecosystems due to extensive use for controlling pests in agriculture has became worldwide concern, while the toxic response of triazophos on the non-target green algae in aquatic environment is not well studied. Therefore, the acute (96 h) toxic effects of 1 and 10 mg/L triazophos on green algae Chlorella pyrenoidosa were evaluated in present study. The results showed that the growth was notably inhibited when treated with triazophos and the 96 h-EC50 (median inhibition concentration) were 12.79 mg/L. The content of photosynthetic pigments (including chl a, chl b, total-chl and carotinoids) clearly decreased under two treatments after 48 h and 96 h with exception for the values at 48 h exposure in 1 mg/L treatment. In addition, the transcript abundance of photosynthesis-related genes (psbA, psbC and rbcL) showed obvious decrease in above two treatments after exposure 96 h to triazophos. In response to 10 mg/L triazophos treatment, the morphology of thylakoid chloroplast of algal cells were obviously damaged. It was also found that starch granules increased with down-regulation of atpB gene expression in 10 mg/L treatment, which suggests that triazophos may inhibit the energy metabolism of C. pyrenoidosa. Moreover, the algal growth inhibition was along with the increase of intracellular reactive oxygen species (ROS), activity of antioxidant enzymes and malondialdehyde content indicating oxidative damage and lipid peroxidation in the algal cells. Our findings reveal that triazophos has potential toxicity and environmental risks to one of the primary producers green algae.

Albicanol inhibits the toxicity of profenofos to grass carp hepatocytes cells through the ROS/PTEN/PI3K/AKT axis.

Profenofos (PFF) as an environmental pollutant seriously harms the health of aquatic animals, and even endangers human safety through the food chain. Albicanol, a sesquiterpenoid extraction from the Dryopteris fragrans, has previously been shown to effectively exhibit anti-aging, anti-oxidant, and antagonize the toxicity of heavy metals. However, the mechanism of hepatocyte toxicity caused by PFF and the role that Albicanol plays in this process are still unclear. In this study, a PFF poisoning model was established by treating grass carp hepatocytes cells with PFF (150 µM) for 24 h The results of AO/EB staining, Tunel staining and flow cytometry showed that the proportion of apoptotic liver cells increased significantly after exposure. The results of ROS staining show that compared with the control group, ROS levels and PTEN/PI3K/AKT-related gene expression were up-regulated after PFF exposure. RT-qPCR and Western blotting results showed that the expression of PTEN/PI3K/AKT related genes was up-regulated. These results indicate that PFF can induce oxidative stress in hepatocytes and inhibit the phosphorylation of AKT. We further found that the expressions of Bax, CytC, Caspase-3, Caspase-9, Caspase-8 and TNFR1 after PFF exposure were significantly higher than those of the control group, and Bcl-2/Bax was significantly lower than that of the control group. These results indicate that PFF can induce oxidative stress in hepatocytes and inhibit the phosphorylation of AKT and activate mitochondrial apoptosis. Using Albicanol (5 × 10-5 µg mL-1) can significantly reduce the above-mentioned effects of PFF exposure on grass carp hepatocytes cells. In summary, Albicanol inhibits PFF-induced apoptosis by regulating the ROS/PTEN/PI3K/AKT pathway.

Osmolal and anion gaps after acute self-poisoning with agricultural formulations of the organophosphorus insecticides profenofos and diazinon: A pilot study.

Self-poisoning with organophosphorus (OP) insecticides is an important means of global self-harm. The insecticides are formulated with solvents that may also contribute to toxicity. We set up a study to detect changes in osmolal and anion gaps following ingestion of OP insecticides. We recruited consecutive patients admitted to a Teaching Hospital, Sri Lanka, with a history of OP self-poisoning. The osmolal and anion gaps were calculated on admission and at 4, 24 and 72 h post-ingestion together with ethanol concentration. Forty-nine patients were recruited (28 profenofos, 10 diazinon, one coumaphos, one chlorpyrifos, one phenthoate and eight unknown OP). Only modest increases in osmolal and anion gaps were noted. Small rises in osmolal gap above the upper limit of normal were noted in 16/49 (32.7%) of all cases, 9/28 (32.1%) profenofos cases and 4/10 (40.0%) diazinon cases. The anion gap was raised in 24/49 (49.0%) of all cases, 15/28 (53.6%) profenofos cases and 5/10 (50.0%) diazinon cases. We observed a trend for a fall in osmolal gap during the first 24 h, followed by an increase up to 72 h. There was no correlation between the anion gap and serum lactate concentration, indicating that a lactic acidosis was not responsible for the anion gap. Formate, which could have explained the increased gap, was not detected in any of the samples; ketoacids (beta-hydroxybutyrate and acetoacetate) were not measured. This pilot study found that profenofos and diazinon poisoning caused only modest increases in the osmolal and anion gaps in a minority of cases.

Triazophos and its metabolite diethyl phosphate have different effects on endocrine hormones and gut health in rats.

Organophosphorus pesticide (OP) residues present in food can be metabolized into diethylphosphate (DEP) in vivo. Epidemiological studies of OPs have usually focused on these metabolites, while animal studies mainly assessed the OPs. Here, we compared the health risks of a frequently detected OP, triazophos (TAP), and its major metabolite, DEP, in rats. Levels of serum lipids and, sex hormones were measured using immunoassay kits. Gut hormones and inflammatory cytokines were assessed using a multiplexing kit, and the gut microbiota was evaluated by 16S rRNA gene sequencing. After a 24-week exposure period, both TAP and DEP significantly decreased serum levels of triglycerides, cholesterol, low-density lipoprotein cholesterol, and IL-6 (p < 0.05). However, DEP exposure had a stronger effect on serum estradiol (p < 0.05) than TAP, whereas only TAP inhibited the secretion of gut hormones. Both TAP and DEP enriched the pathogenic genera Oscillibacter, Peptococcus and Paraprevotella in the gut, and TAP also enriched enteritis-related genera Roseburia and Oscillibacter, which may affect the secretion of gut hormones. These findings indicate that the use of dialkyl phosphates as markers of OPs to examine the correlations of OP exposure with diseases may only provide partial information, especially for diseases related to gut health and the endocrine system.

Three widely used pesticides and their mixtures induced cytotoxicity and apoptosis through the ROS-related caspase pathway in HepG2 cells.

Difenoconazole, cypermethrin and triazophos are widely used pesticides in agricultural production and frequently detected in foods. The aim of this study was to determine the effect of these pesticides and their mixtures on cell viability, reactive oxygen species (ROS), lactate dehydrogenase (LDH) content, apoptosis rate and DNA fragmentation and synthesis in human hepatocellular carcinoma cells (HepG2). The order of inhibitory effects for the individual pesticides was ranked as difenoconazole > cypermethrin > triazophos. The enhanced expression of caspase-3, caspase-7 and PARP activity was observed in HepG2 cells, which was 1.7, 1.3 and 1.6-fold higher than the control, respectively, along with significant protein cleavage; and induced apoptosis in a concentration-dependent manner. Further, the pesticide mixtures significantly increased ROS level (up to 1.3-fold), induced DNA fragmentation (up to 1.8-fold), inhibited DNA synthesis (up to 53%), and damaged the cells by destroying the cell membrane and producing a large amount of LDH at concentration range of 10-30 µM. Specifically, mixtures containing difenoconazole showed stronger toxicities than individual pesticides, implying higher health risks associated with mixtures. Our results show that three widely used pesticides exhibited cytotoxicity and apoptosis through the ROS-related caspase pathway, providing a basis for evaluation of health risks from pesticide mixtures via food consumption.

Evaluation of triazophos induced immunotoxicity of spleen and head kidney in fresh water teleost, Channa punctata.

The utilization of pesticides has increased for destroying pests and protecting crops in the agriculture field. Triazophos is a commonly used organophosphorous insecticide that causes alterations in haematological and histological parameters in fish. The present study was designed to evaluate the effect of triazophos induced innate and cell mediated immunotoxicity in freshwater teleost, Channa punctata. Fishes were exposed to triazophos at concentrations 5 and 10% of LC50 value for 10 and 20 days. Splenic and head kidney macrophage phagocytosis, nitric oxide production and superoxide production were assayed to evaluate the innate immunity. Cell-mediated immunity was measured through splenic and head kidney lymphocyte proliferation in presence of T and B cell mitogens. Results of the present study revealed that macrophage phagocytosis was significantly reduced after in vivo triazophos treatment. Differential suppressive effect of triazophos was also observed where mitogen induced splenic and head kidney lymphocyte proliferations were reduced after 10 and 20 days treatment. Concentration dependent effect of triazophos was observed in in vivo studies where the production of reactive oxygen and nitrogen intermediates were suppressed. This study describes the first investigation of the effect of triazophos on immune functions and will help to determine appropriate ecotoxicity and immunotoxicity in freshwater teleosts.

Prediction of dose-dependent in vivo acetylcholinesterase inhibition by profenofos in rats and humans using physiologically based kinetic (PBK) modeling-facilitated reverse dosimetry.

Organophosphate pesticides (OPs) are known to inhibit acetylcholine esterase (AChE), a critical effect used to establish health-based guidance values. This study developed a combined in vitro-in silico approach to predict AChE inhibition by the OP profenofos in rats and humans. A physiologically based kinetic (PBK) model was developed for both species. Parameter values for profenofos conversion to 4-bromo-2-chlorophenol (BCP) were derived from in vitro incubations with liver microsomes, liver cytosol, and plasma from rats (catalytic efficiencies of 1.1, 2.8, and 0.19 ml/min/mg protein, respectively) and humans (catalytic efficiencies of 0.17, 0.79, and 0.063 ml/min/mg protein, respectively), whereas other chemical-related parameter values were derived using in silico calculations. The rat PBK model was evaluated against literature data on urinary excretion of conjugated BCP. Concentration-dependent inhibition of rat and human AChE was determined in vitro and these data were translated with the PBK models to predicted dose-dependent AChE inhibition in rats and humans in vivo. Comparing predicted dose-dependent AChE inhibition in rats to literature data on profenofos-induced AChE inhibition revealed an accurate prediction of in vivo effect levels. Comparison of rat predictions (BMDL10 of predicted dose-response data of 0.45 mg/kg bw) and human predictions (BMDL10 of predicted dose-response data of 0.01 mg/kg bw) suggests that humans are more sensitive than rats, being mainly due to differences in kinetics. Altogether, the results demonstrate that in vivo AChE inhibition upon acute exposure to profenofos was closely predicted in rats, indicating the potential of this novel approach method in chemical hazard assessment.

Acute toxicity of organophosphate pesticide profenofos, pyrethroid pesticide λ cyhalothrin and biopesticide azadirachtin and their sublethal effects on growth and oxidative stress enzymes in benthic oligochaete worm, Tubifex tubifex.

The present study was aimed to assess the acute toxicity of organophosphate pesticide, profenofos; synthetic pyrethroid pesticide, λ cyhalothrin and biopesticide, azadirachtin and their sublethal effects on growth rate and oxidative stress biomarkers in Tubifex tubifex in vivo. The results showed that 96 h LC50 value of profenofos, λ cyhalothrin and azadirachtin to Tubifex tubifex are 0.59, 0.13 and 82.15 mg L-1 respectively. Pesticide treated worms showed several behavioral abnormalities including increased mucus secretion, erratic movements, wrinkling activity and decreased clumping tendency during acute exposure. The percentage of autotomy increased significantly (p < 0.05) with the increasing concentration of the pesticides at 96 h of exposure. Sublethal concentrations of profenofos (0.059 and 0.118 mg L-1), λ cyhalothrin (0.013 and 0.026 mg L-1) and azadirachtin (8.2 and 16.4 mg L-1) caused significant alterations in growth rate and oxidative stress enzymes in T. tubifex during 14 days exposure period. The growth rate of the pesticide exposed worms decreased significantly (P < 0.05) in a concentration and duration-dependent manner. Superoxide dismutase (SOD), reduced glutathione (GSH), glutathione-s-transferase (GST) and glutathione peroxidase (GPx) demonstrated a noteworthy (p < 0.05) initial induction followed by a subsequent reduction, while catalase (CAT) and malondialdehyde (MDA) exhibited noteworthy induction (p < 0.05) all through the exposure time. Through principal component analysis, correlation matrix, and integrated biomarker response, the effects of profenofos, λ cyhalothrin and azadirachtin on T. tubifex were distinguished. These results indicate that exposure to profenofos, λ cyhalothrin and azadirachtin affect survivability, change the behavioral responses, reduce the growth rate and induce oxidative stress enzymes in T. tubifex.

Simultaneous degradation of triazophos, methamidophos and carbofuran pesticides in wastewater using an Enterobacter bacterial bioreactor and analysis of toxicity and biosafety.

Triazophos (TAP), methamidophos (MAP) and carbofuran (CF) pesticides are highly toxic, soluble and absorbable. Efficient co-degradation of multi-pesticides is rare reported. The objectives of this study were to investigate TAP, MAP and CF co-degradative ability of Enterobacter sp. Z1 and study the degradation mechanisms. Strain Z1 was shown to efficiently co-degrade TAP, MAP and CF when they were used as primary carbon sources. The degradation occurred over a wide range of temperatures, pH values and pesticide concentrations and followed first-order kinetics. Under the optimum conditions (37 °C, pH 7 and 100 mg/L of each pesticide), the degradation efficiencies were 100%, 100%, and 95.3% for TAP, MAP and CF, respectively. In addition, strain Z1 could simultaneously degrade TAP, MAP, CF and total nitrogen in wastewater in a batch bioreactor, with high removal efficiencies of 98.3%, 100%, 98.7% and 100%, respectively. Genomics, proteomics, qRT-PCR and gene overexpression analyses revealed that the degradation mechanisms involved the activities of multiple proteins, among which, organophosphorus hydrolase (Oph) and 3-hydroxyacyl-CoA dehydrogenase (PaaC) are primarily responsible for TAP and MAP degradation, while carbofuran hydrolase (Mcd) and amidohydrolase (RamA) primarily degrade CF. Among these enzymes, PaaC and RamA are newly identified pesticide-degrading enzymes. Toxicity assays of strain Z1 using reporter recombinase gene (recA) and zebrafish showed that there was no accumulation of toxic metabolites during the degradation process. Biosafety test using zebrafish showed that the strain was nontoxic toward zebrafish. Strain Z1 provides a good purification effect for pesticides-containing wastewater and novel microbial pesticide-degrading mechanisms were discovered.

A single dose of the organophosphate triazophos induces fear extinction deficits accompanied by hippocampal acetylcholinesterase inhibition.

Acute organophosphate (OP) poisoning, particularly by suicide attempts, generates high mortality and morbidity. Few studies have systematically addressed the consequences of acute OP intoxication on cognition and memory of survivors. Preclinical evidence suggests that acute OP-induced effects are associated with inhibiting the brain acetylcholinesterase (AChE) enzyme. The OP triazophos has been used worldwide, although its effects on mnemonic processing are yet to be investigated. Based on the above, the present study investigated whether acute triazophos intoxication interferes with the expression and extinction of contextual fear memory in rats. Hippocampal and amygdalar AChE activity and plasma butyrylcholinesterase (BChE) were measured at the end of the experiment to confirm the cholinergic overstimulation. Independent cohorts of animals intoxicated with triazophos were evaluated in the novel object recognition (NOR) test, a less aversive associative memory task. At the dose of 15 mg/kg, triazophos administered immediately after contextual fear conditioning impaired the extinction but not the expression of freezing behavior. Triazophos poisoning induced no changes in the discrimination index in the NOR test. Triazophos inhibited the AChE activity in a time- and brain region-dependent manner. Our findings suggest that fear memory extinction deficits induced by acute triazophos intoxication are accompanied by hippocampal AChE inhibition. The deficient fear extinction associated with acute OP poisoning may represent a behavioral and biochemical phenotype helpful to study mechanisms of neurotoxicity and treatment approach of OP suicide survivors.

Effects of the sea lice bath treatment pharmaceuticals hydrogen peroxide, azamethiphos and deltamethrin on egg-carrying shrimp (Pandalus borealis).

This study investigated effects of sea lice pharmaceuticals on egg-bearing deep-water shrimp (Pandalus borealis). Both mortality and sub-lethal effects (behavior, embryo development, and reproductive output) were studied for each of three pharmaceuticals alone and in different sequential combinations. The most severe effect was observed for deltamethrin where 2 h exposure to 330 times diluted treatment dose (alone and in sequential application with hydrogen peroxide and azamethiphos) induced almost 100% mortality within a few days after exposure. Similar effects were not observed for hydrogen peroxide or azamethiphos. However, sequential treatment of hydrogen peroxide and azamethiphos (2 h exposure to each pharmaceutical; 500 times dilution) resulted in >40% mortality during the first week following treatment. No sub-lethal effects or loss of eggs in female shrimp could be related to exposure to the bath treatments. Future studies should investigate potential sub-lethal effects at exposure concentrations close to the no-effect concentration.

Emerging pesticides responsible for suicide in rural Sri Lanka following the 2008-2014 pesticide bans.

BACKGROUND: Sri Lanka has reduced its overall suicide rate by 70% over the last two decades through means restriction, through a series of government regulations and bans removing highly hazardous pesticides from agriculture. We aimed to identify the key pesticide(s) now responsible for suicides in rural Sri Lanka to provide data for further pesticide regulation. METHODS: We performed a secondary analysis of data collected prospectively during a cluster randomized controlled trial in the Anuradhapura district of Sri Lanka from 2011 to 16. The identity of pesticides responsible for suicides were sought from medical or judicial medical notes, coroners' records, and the person's family. Trend analysis was done using a regression analysis with curve estimation to identify relative importance of key pesticides. RESULTS: We identified 337 suicidal deaths. Among them, the majority 193 (57.3%) were due to ingestion of pesticides while 82 (24.3%) were due to hanging. A specific pesticide was identified in 105 (54.4%) of the pesticide suicides. Ingestion of carbosulfan or profenofos was responsible for 59 (56.2%) of the suicides with a known pesticide and 17.5% of all suicides. The increasing trend of suicides due to carbosulfan and profenofos over time was statistically significant (R square 0.846, F 16.541, p 0.027). CONCLUSION: Ingestion of pesticides remains the most important means of suicides in rural Sri Lanka. The pesticides that were once responsible for most pesticide suicides have now been replaced by carbosulfan and profenofos. Their regulation and replacement in agriculture with less hazardous pesticides will further reduce the incidence of both pesticide and overall suicides in rural Sri Lanka.