Decrease In Acetylcholinesterase Research Articles

Tetrachlorantraniliprole induces neurodevelopmental toxicity through oxidative stress-mediated apoptosis and dysregulation of Wnt signaling pathway.

Tetrachlorantraniliprole (TCTP) is a novel bisamide insecticide and widely used to protect against lepidopteran insect species. However, the application of TCTP in rice fields often leads to water pollution, posing threats to aquatic organisms and potentially to human health. Few studies have assessed the toxic effects of TCTP on aquatic animals. In this study, we used zebrafish as a model organism to evaluate the toxicity of TCTP. Our findings indicated that TCTP adversely affected the development of zebrafish larvae, impacting parameters such as heart rate, body length, and pericardial edema. Exposure to TCTP resulted in the increased embryo mortality along with higher concentrations of the compound. The expression of neurodevelopment-related genes was inhibited in embryos exposed to TCTP. Hematoxylin and eosin (HE) staining revealed that TCTP caused damage to the brain cells of the embryos. Behavioral analysis showed a reduction in activity of the larvaes, which aligned with a decrease in acetylcholinesterase (AChE) activity. Additionally, RNA sequencing (RNA-seq) was employed to elucidate the mechanisms of toxicity. GO and KEGG analysis identified that the pathways were related to oxidative stress, apoptosis and Wnt signaling. We observed an increase of reactive oxygen species (ROS) and Ca²/Mg²-ATPase activity, while antioxidant enzyme activities (SOD, MDA, CAT, Na/K-ATPase and T-ATPase) were significantly decreased in TCTP-exposed groups. Furthermore, TCTP induced brain cells apoptosis, as evidenced by the upregulation of pro-apoptotic genes (bax, p53, TNFα, caspase3 and caspase9) and the downregulation of anti-apoptotic gene (bcl2). Moreover, TCTP increased the expression of genes involved in Wnt signaling pathway. Notably, oxidative stress and neuronal damage induced by TCTP could be mitigated by astaxanthin, an antioxidant. Additionally, IWR-1, an inhibitor of Wnt signaling pathway, effectively alleviated the upregulation of genes associated with TCTP treatment and inhibited oxidative stress-induced apoptosis. In conclusion, this study demonstrated TCTP-induced defects of neurodevelopment and the brain cells in zebrafish larvae which were primarily driven by oxidative stress-induced apoptosis and dysregulation of Wnt signaling pathway. Importantly, these toxic phenotypes can be rescued by treatment with astaxanthin or IWR-1.

The effects of microplastics exposure on quail's hypothalamus: Neurotransmission disturbance, cytokine imbalance and ROS/TGF-β/Akt/FoxO3a signaling disruption

Microplastics (MPs) have become a major focus of environmental toxicology, raising concerns about their potential adverse effects on animal organs and body systems. As these tiny particles infiltrate ecosystems, they may pose risks to the health of organisms across diverse species. In this study, we attempted to examine the neurotoxic effects of MPs exposure on avian hypothalamus by using an animal model-Japanese quail (Coturnix japonica). The quails of 7-day-old were exposed to 0.02 mg/kg, 0.4 mg/kg and 8 mg/kg polystyrene microplastic (PS-MPs) of environmental relevance for 35 days. The results showed PS-MPs exposure did damages to hypothalamic structure characterized by neuron malformation, irregular arrangement and cellular vacuolation after 5-week exposure. PS-MPs exposure also induced Nissl body reduction and dissolution in the hypothalamus. Moreover, the decrease of acetylcholinesterase (AchE) activity and increasing acetylcholine (Ach) indicated that PS-MPs exposure caused hypothalamic neurotransmission disturbance. PS-MPs exposure also led to neuroinflammation by disrupting the balance between proinflammatory and anti-inflammatory cytokines. Moreover, increasing reactive oxygen species (ROS) and malondialdehyde (MDA) generation with reducing antioxidants indicated PS-MPs led to hypothalamic oxidative stress. Additionally, RNA-Seq analysis found that both transforming growth factor-β (TGF-β) signaling and forkhead box O (FoxO) signaling were disturbed in the hypothalamus by PS-MPs exposure. Especially, the increasing ROS led to TGF-β activation and then induced hypothalamic inflammation by nuclear factor κB (NF-κB) activation. The present study concluded that oxidative stress might be an important mechanistic signaling involved in MPs neurotoxicology.

First biochemical and behavioural analysis of the response of the scorpion Urophonius brachycentrus (Thorell: 1876) upon exposure to an organophosphate.

Scorpionism is an increasing public health problem in the world. Although no specific methodology or product is currently available for the control of those arachnids, the use of insecticides could be an effective tool. Chlorpyrifos is one of the insecticides used, but to date, whether scorpions recognise surfaces with that insecticide and how it affects their physiology and/or biochemistry is unknown. In the present study, we observed that scorpions recognise surfaces with 0.51 and 8.59 μg/cm2 of chlorpyrifos and avoid those areas. The 0.51 μg/cm2 concentration produced a decrease in acetylcholinesterase and an increase in catalase, superoxide dismutase and glutathione S-transferase, whereas the 8.59 μg/cm2 concentration evoked a decrease in acetylcholinesterase and an increase in catalase and glutathione S-transferase. Using the comet assay, we observed that the insecticide at 0.17, 0.51 and 8.59 μg/cm2 caused DNA damage. Finally, we found that the insecticide does not generate significant variations in glutathione peroxidase, glutathione reductase, the amount of protein or lipid peroxidation. The present results offer a comprehensive understanding of how scorpions respond, both at the biochemical and behavioural levels, when exposed to insecticides.

Impact of glyphosate-based herbicide exposure through maternal milk on offspring's antioxidant status, neurodevelopment, and behavior.

Glyphosate-based Herbicide (GBH) is a widely used pesticide that functions as a broad-spectrum, non-selective herbicide. Despite advanced research to describe the neurotoxic potential of GBH, the harmful effects on maternal behavior and neurodevelopment of offspring remain unclear. This study was conducted to highlight the effects of GBH on the antioxidant system, anxiety traits, social interaction, and cognitive and sensorimotor functions in pups exposed to 25 or 50mg/l daily via their mother's milk. Concerning the biochemical biomarkers, GBH administered during the early stages of development negatively affected the status of antioxidant enzymes and lipid peroxidation in the brain structures of the pups. Furthermore, our results showed a significant decrease in acetylcholinesterase (AChE) specific activity within the brains of treated pups. The results of the behavioral tests indicated that the treated offspring developed anxiety, memory, and sociability disorders, as evidenced by the Open Field, Y-maze, object recognition task, and social interaction tests. Through neurodevelopmental testing, we also showed sensorimotor impairment (righting reflex and negative geotaxis) and abnormal maternal behavior. Altogether, our study clearly demonstrates that the developing brain is sensitive to GBH.

Neurotoxic Effects of Imidacloprid on <i>Pethia conchonius</i> (Rosy Barb), a Common Freshwater Fish of India

Insecticides are essential to control arthropod pests in agriculture. However, due to their stability and extended half-lives, they contaminate freshwater aquatic systems like lakes, ponds, and rivers by surface run-offs and leaching. Neonicotinoids are a globally used agricultural pesticides that act as an agonist to the nicotinic acetylcholine receptor (nAChRs) and are known to have harmful effects on non-target organisms like fish. This study aimed to determine the neurotoxic, behavioural, and histopathological effect of three sub-lethal concentrations (SLC I, SLC II, and SLC III) of Imidacloprid (IMI), a neonicotinoid, on the freshwater fish Pethia conchonius. Fish were exposed to IMI for 96 hr, during which their behaviour was recorded, and the brain tissues were collected at 24 hr intervals. Compared to the control group, the IMI-exposed fish showed changes in behaviour, such as jerky, erratic swimming, disequilibrium, and mucus secretion. A significant decrease in Acetylcholinesterase (AChE) activity and histopathological damage were recorded in the brain tissues. The severity of damage and decline in activity was both concentration and time-dependent. The AChE inhibition was observed for SLC III after 96 hr (33.70±2.52) compared to control at 96 hr (84.63±4.25). The optic tectum showed detachment in its layers along with necrosis, and vacuolation. The results indicate that IMI is highly neurotoxic which not only inhibits AChE activity but also causes neural damage in the brain leading to a wide range of behavioural alterations.

Proanthocyanidins supplemented diet alter anti-aging-markers and improved lifespan in Drosophila melanogaster model

BackgroundIt is unequivocally believed that phenolics and flavonoids from fruits and vegetables hold robust prevention potentials against age-related disease development through their abundant hydroxyl groups. This study explored the potential neuromuscular enhancement and anti-aging effects of dietary supplemented proanthocyanidins-rich fraction from Tamarindus indica on Drosophila melanogaster model. One- to three-day-old male and female D. melanogaster were fed with a proanthocyanidins-rich fraction-supplemented diet for 7 days at two different concentrations. Following the effective dose determination, longevity assay (rate of survival), behavioral assay (negative geotaxis and eclosion), and biochemical assays (aging and antioxidant enzymes activities) were conducted to assess the fraction’s longevity, antioxidant, and anti-aging effects on D. melanogaster model.ResultThe results showed a significant (p < 0.05) improvement in the rate of emergence and lifespan of the flies fed with proanthocyanidins-rich fraction-supplemented diet at both concentrations (1.5 mg/g and 2.5 mg/g) compared to the normal control. A significant decrease in acetylcholinesterase (AChE) activity and the level of caspase-3 and caspase-9 were observed in the D. melanogaster flies fed with the fraction-containing diet when compared with the normal control. The supplemented diet also significantly increases the activity of catalase, superoxide dismutase (SOD), and glutathione-s-transferase (GST) in a concentration-dependent manner but not nicotinamide quinone oxidoreductase one (NQO1) in D. melanogaster upon comparison with the normal control.ConclusionThe observable changes in the experiment were attributed to the T. indica-derived proanthocyanidins, flavonoids with robust biological activities. The flavonoid-rich fraction proved its potential by enhancing the antioxidant system in D. melanogaster via the increase in the activities of some of the phase II antioxidant enzymes. The present study provides more insights into the wider perspectives of societies on the use of plant-derived natural compounds as the potential approach toward prevention against aging and age-related morbidities which enhance wellness and the quality of life in humans and animals.

Aflatoxin B1-induced redox imbalance in the hippocampus and cerebral cortex of male Wistar rats is accompanied by altered cholinergic, indoleaminergic, and purinergic pathways: Abatement by dietary rutin

The neurotoxic impact of dietary exposure to aflatoxin B1 (AFB1) is well documented in experimental studies. Rutin is a phytochemical with prominent anti-inflammatory and antioxidant activities. There is an information gap on the influence of rutin on AFB1-induced neurotoxicity. This study investigated the influence of rutin on neurobehavioral and biochemical abnormalities in male Wistar rats (six weeks old) orally treated with AFB1 (0.75, and 1.5 mg/kg body weight) or co-administered with rutin (50 mg/kg) for 30 uninterrupted days. Results indicate that AFB1-induced depression-like behavior by Tail Suspension Test (TST) and cognitive impairment by Y-maze was abated following rutin co-administration. Abatement of AFB1-induced decreases in acetylcholinesterase (AChE) activity, and increased antioxidant status, by rutin was accompanied by a marked reduction in oxidative stress markers and increased hydrolysis of the purinergic molecules in the cerebral cortex and hippocampus of rats. Additionally, rutin co-treatment abrogated AFB1-mediated elevation of interleukin-6 (IL-6), nitric oxide (NO) levels, and activity of myeloperoxidase (MPO). Correspondingly, rutin co-treatment lowered the activity and immunocontent of immunosuppressive indoleamine 2, 3-dioxygenase (IDO). Further, rutin co-treatment prevented histological injuries in the cerebral cortex and hippocampus. In conclusion, abatement of AFB1-induced neurobehavioral abnormalities by rutin involves the mechanisms of anti-inflammatory, antioxidant, and regulation of cholinergic, purinergic, and indoleaminergic pathways in rats.

UPLC/ESI/MS profiling of red algae Galaxaura rugosa extracts and its activity against malaria mosquito vector, Anopheles pharoensis, with reference to Danio rerio and Daphnia magna as bioindicators

BackgroundAnopheles pharoensis has a major role in transmitting several human diseases, especially malaria, in Egypt?. Controlling Anopheles is considered as an effective strategy to eliminate the spread of malaria worldwide. Galaxaura rugosa is a species of red algae found in tropical to subtropical marine environments. The presence of G. rugosa is indicative of the ecosystem's overall health. The current work aims to investigate UPLC/ESI/MS profile of G. rugosa methanol and petroleum ether extracts and its activity against An. pharoensis and non-target organisms, Danio rerio and Daphnia magna.MethodsGalaxaura rugosa specimens have been identified using DNA barcoding for the COI gene and verified as G. rugosa. The UPLC/ESI/MS profiling of G. rugosa collected from Egypt was described. The larvicidal and repellent activities of G. rugosa methanol and petroleum ether extracts against An. pharoensis were evaluated, as well as the toxicity of tested extracts on non-target organisms, Dan. rerio and Dap. magna.ResultsThe UPLC/ESI/MS analysis of methanol and petroleum ether extracts led to the tentative identification of 57 compounds belonging to different phytochemical classes, including flavonoids, tannins, phenolic acids, phenyl propanoids. Larval mortality was recorded at 93.33% and 90.67% at 80 and 35 ppm of methanol and petroleum ether extracts, respectively, while pupal mortality recorded 44.44 and 22.48% at 35 and 30 ppm, respectively. Larval duration was recorded at 5.31 and 5.64 days by methanol and petroleum ether extracts at 80 and 35 ppm, respectively. A decrease in acetylcholinesterase (AChE) level and a promotion in Glutathione-S-transferase (GST) level of An. pharoensis 3rd instar larvae were recorded by tested extracts. The petroleum ether extract was more effective against An. pharoensis starved females than methanol extract. Also, tested extracts recorded LC50 of 1988.8, 1365.1, and 11.65, 14.36 µg/mL against Dan. rerio, and Dap. magna, respectively.ConclusionsUsing red algae derivatives in An. pharoensis control could reduce costs and environmental impact and be harmless to humans and other non-target organisms.

Neurotoxicity and the potential molecular mechanisms of mono-2-ethylhexyl phthalic acid (MEHP) in zebrafish

Mono-2-ethylhexyl phthalic acid (MEHP) is the most toxic metabolite of plasticizer di-2-ethylhexyl phthalic acid (DEHP), and there is limited information available on the effects of MEHP on neurotoxicity. This study aims to examine the neurotoxicity of MEHP and preliminarily explore its potential molecular mechanisms. We found that MEHP impeded the growth of zebrafish embryos and the neurodevelopmental-related gene expression at environmentally relevant concentrations. MEHP exposure also induces oxidative stress response and brain cell apoptosis accompanied by a decrease in acetylcholinesterase (AChE) activity in zebrafish larvae. RNA-Seq and bioinformatics analysis showed that MEHP treatment altered the nervous system, neurogenic diseases, and visual perception pathways. The locomotor activity in dark-to-light cycles and phototaxis test confirmed the abnormal neural behavior of zebrafish larvae. Besides, the immune system has produced a large number of differentially expressed genes related to neural regulation. Inflammatory factor IL1β and IL-17 signaling pathways highly respond to MEHP, indicating that inflammation caused by immune system imbalance is a potential mechanism of MEHP-induced neurotoxicity. This study expands the understanding of the toxicity and molecular mechanisms of MEHP, providing a new perspective for in-depth neurotoxicity exploration of similar compounds.

Effect of insecticides on locomotory behaviour and enzyme activity of Spodoptera litura (Fabricius) populations from Punjab

Aim: The variations in locomotory behaviour and enzyme activity, i.e., acetylcholinesterase and general esterases of Spodoptera litura Fabricius larval populations collected from different regions of Punjab, i.e., Amritsar, Kapurthala and Ludhiana were investigated in the laboratory prior exposure to different insecticides. Methodology: The test larvae were exposed to sublethal doses of different insecticides via surface and food treatment. For locomotory behaviour, they were allowed to move on treated surface and their movements were recorded with an automated video tracking system, Ethovision while on other hand food treatment was opted for observing the influence on enzyme activity. Results: The pronounced variations were observed in the locomotor behaviour of S. litura upon surface exposure of different insecticides. The larva travelled more distance with higher speed and larger turn angle on insecticide-treated surfaces than the untreated ones, while on comparison of different larval populations, the Amritsar population larvae travelled less distance with low speed and maximum turnings. The decrease in acetylcholinesterase and general esterase activity was recorded in treated larvae than untreated ones. The influence of emamectin benzoate was recorded more on locomotion and enzyme activity of S. litura as compared to the remaining insecticides and the Amritsar population was least affected. Interpretation: The sublethal doses of insecticides influenced the overall behavioural physiology of S. litura and this biological parameter could be useful in designing the management strategies for S. litura. Key words: Acetylcholinesterase, Esterases, Insecticides, Locomotory behaviour, S. litura

Possible Interaction between ZnS Nanoparticles and Phosphonates on Mediterranean Clams Ruditapes decussatus.

This study aims to evaluate the toxicity of ZnS nanoparticles (ZnS NP50 = 50 µg/L and ZnS NP100 = 100 µg/L) and diethyl (3-cyano-1-hydroxy-2-methyl-1-phenylpropyl)phosphonate or P (P50 = 50 µg/L and P100 = 100 µg/L) in the clams Ruditapes decussatus using chemical and biochemical approaches. The results demonstrated that clams accumulate ZnS NPs and other metallic elements following exposure. Moreover, ZnS NPs and P separately lead to ROS overproduction, while a mixture of both contaminants has no effect. In addition, data showed that exposure to P100 resulted in increased levels of oxidative stress enzyme activities catalase (CAT) in the gills and digestive glands. A similar trend was also observed in the digestive glands of clams treated with ZnS100. In contrast, CAT activity was decreased in the gills at the same concentration. Exposure to ZnS100 and P100 separately leads to a decrease in acetylcholinesterase (AChE) levels in both gills and digestive glands. Thus, AChE and CAT after co-exposure to an environmental mixture of nanoparticles (ZnS100) and phosphonate (P100) did not show any differences between treated and non-treated clams. The outcome of this work certifies the use of biomarkers and chemical assay when estimating the effects of phosphonate and nanoparticles as part of an ecotoxicological assessment program. An exceptional focus was given to the interaction between ZnS NPs and P. The antioxidant activity of P has been demonstrated to have an additive effect on metal accumulation and antagonistic agents against oxidative stress in clams treated with ZnS NPs.

Toxicity of the 3,4-Methylenedioxymethamphetamine and Its Enantiomers to Daphnia magna after Isolation by Semipreparative Chromatography.

MDMA (3,4-methylenedioxymethamphetamine) is a chiral psychoactive recreational drug sold in illicit markets as racemate. Studies on the impact of MDMA on aquatic organisms are scarce. While enantioselectivity in toxicity in animals and humans has been reported, none is reported on aquatic organisms. This study aimed to investigate the ecotoxicological effects of MDMA and its enantiomers in Daphnia magna. For that, enantiomers (enantiomeric purity > 97%) were separated by liquid chromatography using a homemade semipreparative chiral column. Daphnids were exposed to three concentrations of (R,S)-MDMA (0.1, 1.0 and 10.0 µg L-1) and two concentrations of (R)- and (S)-enantiomers (0.1 and 1.0 µg L-1) over the course of 8 days. Morphophysiological responses were dependent on the substance form and daphnia development stage, and they were overall not affected by the (R)-enantiomer. Changes in swimming behaviour were observed for both the racemate and its enantiomers, but enantioselective effects were not observed. Reproductive or biochemical changes were not observed for enantiomers whereas a significant decrease in acetylcholinesterase and catalase activity was noted at the highest concentration of (R,S)-MDMA (10 µg L-1). Overall, this study showed that sub-chronic exposure to MDMA racemate and its enantiomers can interfere with morphophysiological and swimming behaviour of D. magna. In general, the (R)-enantiomer demonstrated less toxicity than the (S)-enantiomer.

Exploring Mannosylpurines as Copper Chelators and Cholinesterase Inhibitors with Potential for Alzheimer's Disease.

Alzheimer's Disease (AD) is characterized by a progressive cholinergic neurotransmission imbalance, with a decrease of acetylcholinesterase (AChE) activity followed by a significant increase of butyrylcholinesterase (BChE) in the later AD stages. BChE activity is also crucial for the development of Aβ plaques, the main hallmarks of this pathology. Moreover, systemic copper dyshomeostasis alters neurotransmission leading to AD. In the search for structures targeting both events, a set of novel 6-benzamide purine nucleosides was synthesized, differing in glycone configuration and N7/N9 linkage to the purine. Their AChE/BChE inhibitory activity and metal ion chelating properties were evaluated. Selectivity for human BChE inhibition required N9-linked 6-deoxy-α-d-mannosylpurine structure, while all three tested β-d-derivatives appeared as non-selective inhibitors. The N9-linked l-nucleosides were cholinesterase inhibitors except the one embodying either the acetylated sugar or the N-benzyl-protected nucleobase. These findings highlight that sugar-enriched molecular entities can tune bioactivity and selectivity against cholinesterases. In addition, selective copper chelating properties over zinc, aluminum, and iron were found for the benzyl and acetyl-protected 6-deoxy-α-l-mannosyl N9-linked purine nucleosides. Computational studies highlight molecular conformations and the chelating molecular site. The first dual target compounds were disclosed with the perspective of generating drug candidates by improving water solubility.

As natural phytocide: Biomarker assessment of Litsea cubeba (Lour.) Persoon essential oil against Drosophila suzukii Matsumura (Diptera: Drosophilidae.)

The essential oil of Litsea cubeba (Lour.) Pers. (LCEO) has applications as a health and food additive. The study objectives were to demonstrate the toxicity of LCEO against Drosophila and to investigate the essential oil’s mechanism of action. The repellency percentage, fumigation effect and contact activity were all positively correlated with the LCEO concentration, and 1.0 μL/cm2 essential oil repelled Drosophila for 10 min and reached the highest repellant level. Damage to Drosophila organ tissues was assessed by light microscopy, using histological sections to further analyze the mechanism of lethality and treated larvae underwent ultrastructural evaluations. A 6.7-fold decrease in acetylcholinesterase and a 2.7-fold increase in superoxide dismutase indicated significant enzymatic changes, and the two main essential oil action mechanisms on Drosophila were identified, namely neurotoxicity in larvae owing to altered enzyme activities and death owing to homeostatic disruptions by aldehyde oxidation reactions. The phytochemistry of LCEO has broad applications in fruit pest control.

Prolonged fluoride exposure alters neurotransmission and oxidative stress in the zebrafish brain

Fluoride is an essential chemical found in dental preparations, pesticides and drinking water. Excessive fluoride exposure is related to toxicological and neurological disruption. Zebrafish are used in translational approaches to understand neurotoxicity in both biomedical and environmental areas. However, there is no complete knowledge about the cumulative effects of fluoride on neurotransmission systems. Therefore, the aim of this study was to evaluate whether prolonged exposure to sodium fluoride (NaF) alters cholinergic and glutamatergic systems and oxidative stress homeostasis in the zebrafish brain. Adult zebrafish were used, divided into four experimental groups, one control group and three groups exposed to NaF at 30, 50 and 100 mg.L−1 for a period of 30 days. After NaF at 30 mg.L−1 exposure, there were significant decreases in acetylcholinesterase (29.8 %) and glutamate uptake (39.3 %). Furthermore, thiobarbituric acid-reactive species were decreased at NaF 50 mg.L-1 (32.7 %), while the group treated with NaF at 30 mg.L−1 showed an increase in dichlorodihydrofluorescein oxidation (41.4 %). NaF at 30 mg.L-1 decreased both superoxide dismutase (55.3 %) and catalase activities (26.1 %). The inhibitory effect observed on cholinergic and glutamatergic signalling mechanisms could contribute to the neurodegenerative events promoted by NaF in the zebrafish brain.

Developmental neurotoxicity of antimony (Sb) in the early life stages of zebrafish

Accumulating studies have revealed the toxicity of antimony (Sb) to soil-dwelling and aquatic organisms at the individual level. However, little is known about the neurotoxic effects of antimony and its underlying mechanisms. To assess this issue, we investigated the neurotoxicity of antimony (0, 200, 400, 600 and 800 mg/L) in zebrafish embryos. After exposure, zebrafish embryos showed abnormal phenotypes such as a shortened body length, morphological malformations, and weakened heart function. Behavioral experiments indicated that antimony caused neurotoxicity in zebrafish embryos, manifested in a decreased spontaneous movement frequency, delayed response to touch, and reduced movement distance. We also showed that antimony caused a decrease in acetylcholinesterase (AChE) levels in zebrafish embryos, along with decreased expression of neurofunctional markers such as gfap, nestin, mbp, and shha. Additionally, antimony significantly increased reactive oxygen species levels and significantly reduced glutathione (GSH) and superoxide dismutase (SOD) activity. In summary, our findings indicated that antimony can induce developmental toxicity and neurotoxicity in zebrafish embryos by affecting neurotransmitter systems and oxidative stress, thus altering behavior. These outcomes will advance our understanding of antimony-induced neurotoxicity, environmental problems, and health hazards.

Neuroprotective action of aspirin on Paraquat intoxication in on Drosophila melanogaster

Acetylsalicylic acid or aspirin is the most widely used drug globally for its anti-inflammatory characteristics, although little is known about its actions on the central nervous system (CNS). We investigated aspirin's potential neuroprotective effects against paraquat-induced neurotoxicity (PQ) in the present study. Adult male wild-type flies were exposed to a diet containing PQ (3 mM) and/or aspirin (1 μM; 5 μM; 10 μM). Flies fed with PQ reduced locomotion and increased mortality. PQ-induced neurotoxicity has also been associated with a marked decrease in acetylcholinesterase (AChE) activity and lipid peroxidation. Co-exposure to aspirin (5 μM) increased survival, improved motor performance, increased AChE activity, and decreased lipid peroxidation. Our results suggest aspirin's neuroprotective effects, probably due to its lysosomal action and antioxidant characteristics. Thus, we demonstrate that the Drosophila melanogaster model can elucidate basic aspirin mechanisms to assist the evaluations carried out in higher animals to minimize the neurodegenerative effects caused by diseases such as Parkinson's and Alzheimer's.

Chronic ciprofloxacin and atrazine co-exposure aggravates locomotor and exploratory deficits in non-target detritivore speckled cockroach (Nauphoeta cinerea).

The global detection of ciprofloxacin and atrazine in soil is linked to intensive anthropogenic activities in agriculture and inadvertent discharge of industrial wastes to the environment. Nauphoeta cinerea is a terrestrial insect with cosmopolitan distribution and great environmental function. The current study probed the neurobehavioral and cellular responses of N. cinerea singly and jointly exposed to atrazine (1.0 and 0.5μgg-1 feed) and ciprofloxacin (0.5 and 0.25μgg-1 feed) for 63days. Results demonstrated that the reductions in the body rotation, maximum speed, turn angle, path efficiency, distance traveled, episodes, and time of mobility induced by atrazine or ciprofloxacin per se was exacerbated in the co-exposure group. The altered exploratory and locomotor in insects singly and jointly exposed to ciprofloxacin and atrazine were verified by track plots and heat maps. Furthermore, we observed a decrease in acetylcholinesterase and anti-oxidative enzyme activities with concomitant elevation in the levels of lipid peroxidation, nitric oxide, and reactive oxygen and nitrogen species were significantly intensified in the midgut, hemolymph, and head of insects co-exposed to ciprofloxacin and atrazine. In conclusion, exposure to binary mixtures of ciprofloxacin and atrazine elicited greater locomotor and exploratory deficits than upon exposure to the individual compound by inhibiting acetylcholinesterase activity and induction of oxido-inflammatory stress responses in the insects. N. cinerea may be a usable model insect for checking contaminants of ecological risks.

Gallic Acid Reverses Neurochemical Changes Induced by Prolonged Ethanol Exposure in the Zebrafish Brain

Gallic acid (GA) is a polyphenolic compound that has attracted significant interest due to its antioxidant action through free radical elimination and metal chelation. Ethanol is a highly soluble psychoactive substance, and its toxicity is associated with oxidative stress. In this context, the purpose of the present study was to investigate the effect of GA on neurochemical changes in zebrafish brains exposed to ethanol. GA was first analyzed in isolation by treating the animals at concentrations of 5, 10, and 20 mg/L for 24 h and 48 h. The results revealed that the group exposed to 20 mg/L over a 24/48 h period exhibited increases in thiobarbituric acid reactive substance (TBA-RS) levels and 2′,7′-dichlorofluorescein (DCFH) oxidation, demonstrating a pro-oxidant profile. Moreover, decrease in acetylcholinesterase (AChE) enzyme activity was observed. To investigate the effects of GA after ethanol exposure, the animals were divided into four groups: control; those exposed to 0.5% ethanol for 7 days; those exposed to 0.5% ethanol for 7 days and treated with GA at 5 and 10 mg/L on day 8. Treatment with GA at 5 and 10 mg/L reversed impairment of choline acetyltransferase activity and the damage to TBA-RS levels, DCFH oxidation, and superoxide dismutase activity induced by ethanol. Results of the present study suggest that GA treatment (20 mg/L) appeared to disrupt oxidative parameters in the zebrafish brain. GA treatment at 5 and 10 mg/L reversed alterations to the cholinergic system induced by prolonged exposure to ethanol in the zebrafish brain, probably through an antioxidant mechanism.

Acute exposure to chlorpyrifos and glyphosate induces changes in hemolymph biochemical parameters in the crayfish, Astacus leptodactylus (Eschscholtz, 1823)

Acute and subacute toxicity tests for chlorpyrifos and glyphosate were performed on the crayfish, Astacus leptodactylus. The crayfish were divided into a control group and four experimental groups with exposure from 50.18 to 301.11 μg L−1 of chlorpyrifos for 96 h under semi-static test conditions. In the same experiment, the crayfish were exposed to different concentrations of glyphosate (from 0.0, 8.14 to 13.05 mg L−1) for 96 h. Mortality was recorded, and the median lethal concentrations (LC50) were calculated using probit analysis. The 96 h LC50 values of chlorpyrifos and glyphosate to A. leptodactylus were 49.55 ± 4.66 μg L−1 and 7.83 ± 0.50 mg L−1, respectively. The results showed that chlorpyrifos was a few hundred times more toxic than glyphosate for the crayfish. Then, the crayfish were exposed to different subacute concentrations of chlorpyrifos (12.5 and 25 μg L−1) and glyphosate (2 mg L−1 and 4 mg L−1) for seven days, and their toxicity was evaluated through several hemolymph biochemical parameters. Chlorpyrifos and glyphosate exposure caused a significant (P < 0.01) increase in the activity of lactate dehydrogenase (LDH), and gamma-glutamyl transferase (GGT). The results showed a significant (P < 0.01) decrease in acetylcholinesterase (AChE), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and phenoloxidase (PO) activities in the hemolymph of the crayfish exposed to chlorpyrifos and glyphosate. The total protein and cholesterol levels showed a significant decrease (P < 0.01) in the hemolymph of the crayfish after seven days of exposure to chlorpyrifos and glyphosate. There was a significant increase in triglycerides and glucose levels in treated crayfish. These results show that chlorpyrifos is highly toxic, while glyphosate is moderately toxic to A. leptodactylus. According to the results, subacute concentrations of chlorpyrifos and glyphosate could lead to a collapse of cellular homeostasis and changes in the hemolymph biochemical parameters in the crayfish. Physiological changes caused by exposure to chlorpyrifos and glyphosate in A. leptodactylus may have direct effects on the survival of these organisms.