Pesticide Toxicity https://greenmedinfo.com/category/keywords/Pesticide%20Toxicity en Chlorpyrifos can decrease the viability of adipose tissue-derived stem cells-derived neurons and dysregulate the expression of some neuronal markers. https://greenmedinfo.com/article/chlorpyrifos-can-decrease-viability-adipose-tissue-derived-stem-cells-derived- n/a PMID:  Environ Toxicol. 2016 Nov ;31(11):1510-1519. Epub 2015 May 27. PMID: 26018426 Abstract Title:  Study of the chlorpyrifos neurotoxicity using neural differentiation of adipose tissue-derived stem cells. Abstract:  Chlorpyrifos (CPF) is the most commonly used organophosphorus insecticide which causes neurodevelopmental toxicity. So far, animals have been used as ideal models for neurotoxicity studies, but working with animals is very expensive, laborious, and ethically challenging. This has encouraged researchers to seek alternatives. During recent years, several studies have reported successful differentiation of embryonic and adult stem cells to neurons. This has provided an excellent model for neurotoxicologic studies. In this study, neural differentiation of mouse adipose tissue-derived stem cells (ADSCs) was used as an in vitro model for investigation of CPF neurotoxicity. For this purpose, mouse ADSCs were cultured in a medium containing knockout serum replacement and were treated with different concentrations of CPF at several stages of differentiation. Cytotoxic effect of CPF and the expression of neuron-specific genes and proteins were studied in the differentiating ADSCs. Furthermore, the activity of acetylcholinesterase was assessed by Ellman assay at different stages of differentiation. This study showed that up to 500μM CPF did not alter viability of the undifferentiated ADSCs, whereas viability of the differentiating cells decreased with 500 μM CPF. CPF upregulated the expression of some neuron-specific genes and seemed to decrease the number of β-tubulin III and MAP2 proteins-expressing cells. There was nodetectable acetylcholine esterase activity in differentiated ADSCs. In summary, it was shown that CPF treatment can decrease the viability of ADSC-derived neurons and dysregulate the expression of some neuronal markers through acetylcholinesterase-independent mechanisms. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1510-1519, 2016. https://greenmedinfo.com/article/chlorpyrifos-can-decrease-viability-adipose-tissue-derived-stem-cells-derived-#comments Neurodegenerative Diseases Pesticide Toxicity Chlorpyrifos Chlorpyrifos Neurodegenerative diseases Pesticide Toxicity In Vitro Study Fri, 18 Aug 2017 14:35:32 +0000 greenmedinfo 151856 at https://greenmedinfo.com Chlorpyrifos may affect neurodevelopment in a manner similar to that of several known and suspected neurotoxicants. https://greenmedinfo.com/article/chlorpyrifos-may-affect-neurodevelopment-manner-similar-several-known-and-susp n/a PMID:  Neurotoxicology. 2014 May ;42:58-70. Epub 2014 Apr 12. PMID: 24727577 Abstract Title:  Nuclear NF-κB contributes to chlorpyrifos-induced apoptosis through p53 signaling in human neural precursor cells. Abstract:  Chlorpyrifos (CPF) is one of the most widely used organophosphate insecticides with several harmful effects, including neurotoxicity. Although many studies have addressed the neurotoxicity induced by CPF, most data on neurodevelopmental damage was obtained from animal models. We are the first group to use human neural precursor cells (hNPCs) derived from human embryonic stem cells (hESCs) as a developing neuron model to evaluate the mechanisms involved in CPF-induced neurotoxicity. CPF was cytotoxic to these cells in a concentration-dependent manner, as shown by decreased cell viability and increased lactate dehydrogenase release. Furthermore, CPF reduced the expression of AKT and ERK proteins which are involved in intracellular survival pathways. Exposure of hNPCs to CPF led to the production of reactive oxygen species (ROS), and the antioxidant N-acetyl-cystein (NAC) attenuated ROS production induced by CPF. In addition, CPF increased cytochrome c release into the cytosol and activated caspase-9 and -3, indicating that cell death induced by CPF was due to apoptosis in hNPCs. Consistent with these findings, CPF treatment reduced the level of Bcl-2 protein and increased the level of Bax protein. Especially, CPF increased the translocation of BAX into the mitochondria. CPF also induced nuclear accumulation of NF-κB and p53 proteins in a concentration-dependent manner, and their inhibitors attenuated CPF-induced cytotoxicity. In addition, an inhibitor of NF-κB nuclear translocation blocked the increase of p53 in CPF-treated hNPCs. These findings show that CPF induced hNPCs death in part through NF-κB activation via ROS generation, enabling the interaction of p53 with Bcl-2 and Bax and subsequent release of cytochrome c. Collectively, these results represent a unique molecular characterization of CPF-induced cytotoxicity in hNPCs. These data suggest that CPF may affect neurodevelopment in a manner similar to that of several known and suspected neurotoxicants. https://greenmedinfo.com/article/chlorpyrifos-may-affect-neurodevelopment-manner-similar-several-known-and-susp#comments Oxidative Stress Pesticide Toxicity Chlorpyrifos Chlorpyrifos oxidative stress Pesticide Toxicity In Vitro Study Fri, 18 Aug 2017 15:13:21 +0000 greenmedinfo 151860 at https://greenmedinfo.com Developmental neurotoxicity of the organophosphorus insecticide chlorpyrifos. https://greenmedinfo.com/article/developmental-neurotoxicity-organophosphorus-insecticide-chlorpyrifos n/a PMID:  J Neurochem. 2017 Aug ;142 Suppl 2:162-177. PMID: 28791702 Abstract Title:  Developmental neurotoxicity of the organophosphorus insecticide chlorpyrifos: from clinical findings to preclinical models and potential mechanisms. Abstract:  Organophosphorus (OP) insecticides are pest-control agents heavily used worldwide. Unfortunately, they are also well known for the toxic effects that they can trigger in humans. Clinical manifestations of an acute exposure of humans to OP insecticides include a well-defined cholinergic crisis that develops as a result of the irreversible inhibition of acetylcholinesterase (AChE), the enzyme that hydrolyzes the neurotransmitter acetylcholine (ACh). Prolonged exposures to levels of OP insecticides that are insufficient to trigger signs of acute intoxication, which are hereafter referred to as subacute exposures, have also been associated with neurological deficits. In particular, epidemiological studies have reported statistically significant correlations between prenatal subacute exposures to OP insecticides, including chlorpyrifos, and neurological deficits that range from cognitive impairments to tremors in childhood. The primary objectives of this article are: (i) to address the short- and long-term neurological issues that have been associated with acute and subacute exposures of humans to OP insecticides, especially early in life (ii) to discuss the translational relevance of animal models of developmental exposure to OP insecticides, and (iii) to review mechanisms that are likely to contribute to the developmental neurotoxicity of OP insecticides. Most of the discussion will be focused on chlorpyrifos, the top-selling OP insecticide in the United States and throughout the world. These points are critical for the identification and development of safe and effective interventions to counter and/or prevent the neurotoxic effects of these chemicals in the developing brain. This is an article for the special issue XVth International Symposium on Cholinergic Mechanisms. https://greenmedinfo.com/article/developmental-neurotoxicity-organophosphorus-insecticide-chlorpyrifos#comments Pesticide Toxicity Chlorpyrifos Neurotoxic Chlorpyrifos Pesticide Toxicity Review Fri, 18 Aug 2017 15:28:09 +0000 greenmedinfo 151863 at https://greenmedinfo.com Low-dose pesticide mixture induces senescence in normal mesenchymal stem cells (MSC) and promotes tumorigenic phenotype in premalignant MSC. https://greenmedinfo.com/article/low-dose-pesticide-mixture-induces-senescence-normal-mesenchymal-stem-cells-ms n/a PMID:  Stem Cells. 2017 Mar ;35(3):800-811. Epub 2016 Nov 23. PMID: 27860054 Abstract Title:  Low-Dose Pesticide Mixture Induces Senescence in Normal Mesenchymal Stem Cells (MSC) and Promotes Tumorigenic Phenotype in Premalignant MSC. Abstract:  Humans are chronically exposed to multiple environmental pollutants such as pesticides with no significant evidence about the safety of such poly-exposures. We exposed mesenchymal stem cells (MSC) to very low doses of mixture of seven pesticides frequently detected in food samples for 21 days in vitro. We observed a permanent phenotype modification with a specific induction of an oxidative stress-related senescence. Pesticide mixture also induced a shift in MSC differentiation towards adipogenesis but did not initiate a tumorigenic transformation. In modified MSC in which a premalignant phenotype was induced, the exposure to pesticide mixture promoted tumorigenic phenotype both in vitro and in vivo after cell implantation, in all nude mice. Our results suggest that a common combination of pesticides can induce a premature ageing of adult MSC, and as such could accelerate age-related diseases. Exposure to pesticide mixture may also promote the tumorigenic transformation in a predisposed stromal environment. Abstract Video Link: https://youtu.be/mfSVPTol-Gk Stem Cells 2017;35:800-811. https://greenmedinfo.com/article/low-dose-pesticide-mixture-induces-senescence-normal-mesenchymal-stem-cells-ms#comments Aging Cancers: All Pesticide Toxicity Pesticides Aging Cancer Stem Cells Cancers: All Mesenchymal Stem Cells Pesticide Toxicity pesticides Animal Study In Vitro Study Fri, 18 Aug 2017 14:10:15 +0000 greenmedinfo 151853 at https://greenmedinfo.com Naringenin exerts anti-inflammatory effects in paraquat-treated SH-SY5Y cells. https://greenmedinfo.com/article/naringenin-exerts-anti-inflammatory-effects-paraquat-treated-sh-sy5y-cells n/a PMID:  Neurochem Res. 2018 Feb 6. Epub 2018 Feb 6. PMID: 29411263 Abstract Title:  Naringenin Exerts Anti-inflammatory Effects in Paraquat-Treated SH-SY5Y Cells Through a Mechanism Associated with the Nrf2/HO-1 Axis. Abstract:  Naringenin (NGN; 5,7-dihydroxy-2-(4-hydroxyphenyl)-2,3-dihydrochromen-4-one; CHO), a flavanone, is found in citrus fruits and has been viewed as an antioxidant and anti-inflammatory agent. NGN is a potent inducer of the nuclear factor erythroid 2-related factor 2 (Nrf2) and upregulates the expression of heme oxygenase-1 (HO-1), an enzyme exhibiting both antioxidant and anti-inflammatory effects. The complete mechanism by which NGN exerts anti-inflammatory actions is not completely understood yet. Therefore, we investigated here whether NGN would be able to reduce the inflammation induced by paraquat (PQ) in SH-SY5Y cells. Additionally, we analyzed the mechanism associated with the NGN-induced anti-inflammatory effect. We found that a pretreatment with NGN at 80 µM for 2 h decreased the levels of pro-inflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in PQ-treated SH-SY5Y cells. The production of nitric oxide (NO) and levels of cyclooxygenase-2 (COX-2) and of the inducible isoform of nitric oxide synthase (iNOS) were downregulated by NGN in the cells exposed to PQ. Moreover, NGN downregulated the activation of the nuclear factor-κB (NF-κB) in PQ-treated cells. The anti-apoptotic and anti-inflammatory effects promoted by NGN were abolished by ZnPP IX (a specific inhibitor of HO-1) or by knockdown of Nrf2 by small interfering RNA (siRNA). Therefore, NGN induced anti-inflammatory effects in PQ-treated SH-SY5Y cells by a mechanism associated with the Nrf2/HO-1 signaling pathway. https://greenmedinfo.com/article/naringenin-exerts-anti-inflammatory-effects-paraquat-treated-sh-sy5y-cells#comments Naringenin Pesticide Toxicity Anti-Inflammatory Agents Cyclooxygenase 2 Inhibitors Heme oxygenase-1 up-regulation Interleukin-1 beta downregulation Nitric Oxide Inhibitor Nrf2 activation Tumor Necrosis Factor (TNF) Alpha Inhibitor Anti-Inflammatory Agents Naringenin Pesticide Toxicity In Vitro Study Sat, 10 Mar 2018 03:34:09 +0000 greenmedinfo 161006 at https://greenmedinfo.com Paraquat inhibited differentiation in human neural progenitor cells. https://greenmedinfo.com/article/paraquat-inhibited-differentiation-human-neural-progenitor-cells n/a PMID:  Environ Toxicol Pharmacol. 2016 Mar ;42:205-11. Epub 2016 Jan 25. PMID: 26878281 Abstract Title:  Paraquat inhibited differentiation in human neural progenitor cells (hNPCs) and down regulated miR-200a expression by targeting CTNNB1. Abstract:  Paraquat (PQ) exposure influences central nervous system and results in serious neurotoxicity in vitro and in vivo. However, the role of PQ exposure in the development of CNS remains unclear. In present study, we investigated microRNAs (miRNAs) expression profiling and cell differential status following PQ treatment in human neural progenitor cells (hNPCs) as well as involved mechanism. Microarray profiling of miRNAs expression of PQ treated cell line and their corresponding control was determined. Differentially expression miRNAs were confirmed by quantitative real time PCR. Neural cell differentiation was performed with immunocytochemical analysis. Predicated target of miRNA was identified with luciferase reports and quantitatively analyzed using western blotting. Our results found PQ dramatically suppressed neural cell differentiation ability. 43 differentially expressed miRNAs were identified in PQ treated cells. The expression levels were over expressed in 25 miRNAs, whereas 18 miRNAs were suppressed. More importantly, we observed that miR-200a expression level to be lower in PQ treated cells. Luciferase assay and protein expression results confirmed the direct binding effect between CTNNB1 and miR-200a following PQ exposure. Collectively, our data suggested that down regulation of miR-200a in the PQ treated neural stem cell significantly participated in the differentiation processes and subsequently resulting in decreased cell viability, increased epithelial-mesenchymal transition process and the inhibited differential through CTNNB1 pathway. https://greenmedinfo.com/article/paraquat-inhibited-differentiation-human-neural-progenitor-cells#comments Pesticide Toxicity Paraquat paraquat Pesticide Toxicity In Vitro Study Fri, 18 Aug 2017 14:49:56 +0000 greenmedinfo 151857 at https://greenmedinfo.com Prenatal organophosphate insecticide exposure effects infant sensory function. https://greenmedinfo.com/article/prenatal-organophosphate-insecticide-exposure-effects-infant-sensory-function n/a PMID:  Int J Hyg Environ Health. 2018 Feb 2. Epub 2018 Feb 2. PMID: 29402694 Abstract Title:  Prenatal organophosphate insecticide exposure and infant sensory function. Abstract:  BACKGROUND: Occupational studies suggest that exposure to organophosphate insecticides (OPs) can lead to vision or hearing loss. Yet the effects of early-life exposure on visual and auditory function are unknown. Here we examined associations between prenatal OP exposure and grating visual acuity (VA) and auditory brainstem response (ABR) during infancy. METHODS: 30 OPs were measured in umbilical cord blood using gas chromatography tandem mass spectrometry in a cohort of Chinese infants. Grating visual acuity (VA) (n = 179-200) and auditory brainstem response (ABR) (n = 139-183) were assessed at 6 weeks, 9 months, and 18 months. Outcomes included VA score, ABR wave V latency and central conduction time, and head circumference (HC). Associations between sensory outcomes during infancy and cord OPs were examined using linear mixed models. RESULTS: Prenatal chlorpyrifos exposure was associated with lower 9-month grating VA scores; scores were 0.64 (95% CI: -1.22, -0.06) points lower for exposed versus unexposed infants (p = 0.03). The OPs examined were not associated with infant ABR latencies, but chlorpyrifos and phorate were both significantly inversely associated with HC at 9 months; HCs were 0.41 (95% CI: 0.75, 0.6) cm and 0.44 (95% CI: 0.88, 0.1) cm smaller for chlorpyrifos (p = 0.02) and phorate (p = 0.04), respectively. CONCLUSIONS: We found deficits in grating VA and HC in 9-month-old infants with prenatal exposure to chlorpyrifos. The clinical significance of these small but statistically significant deficits is unclear. However, the disruption of visual or auditory pathway maturation in infancy could potentially negatively affect downstream cognitive development. https://greenmedinfo.com/article/prenatal-organophosphate-insecticide-exposure-effects-infant-sensory-function#comments Pesticide Toxicity Prenatal Chemical Exposures Pesticides Pesticide Toxicity pesticides Prenatal Chemical Exposures Human Study Thu, 08 Feb 2018 02:31:58 +0000 greenmedinfo 159473 at https://greenmedinfo.com