Pesticides at brain borders: Impact on the blood-brain barrier, neuroinflammation, and neurological risk trajectories.

Persistent organic pollutants (POPs) are organic chemical substances that are widely distributed in environments around the globe. POPs accumulate in living organisms and are found at high concentrations in the food chain. Humans are thus continuously exposed to these chemical substances, in which they exert hepatic, reproductive, developmental, behavioral, neurologic, endocrine, cardiovascular, and immunologic adverse health effects. However, considerable information is unknown regarding the mechanism by which POPs exert their adverse effects in humans, as well as the molecular and cellular responses involved. Data are notably lacking concerning the consequences of acute and chronic POP exposure on changes in gene expression, protein profile, and metabolic pathways. We conducted a systematic review to provide a synthesis of knowledge of POPs arising from proteomics-based research. The data source used for this review was PubMed. This study was carried out following the PRISMA guidelines. Of the 742 items originally identified, 89 were considered in the review. This review presents a comprehensive overview of the most recent research and available solutions to explore proteomics datasets to identify new features relevant to human health. Future perspectives in proteomics studies are discussed.

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Studying the Impact of Persistent Organic Pollutants Exposure on Human Health by Proteomic Analysis: A Systematic Review

Towards regulation of Endocrine Disrupting chemicals (EDCs) in water resources using bioassays – A guide to developing a testing strategy

A metabolomic study on the gender-dependent effects of maternal exposure to fenvalerate on neurodevelopment in offspring mice

Chemicals are comprehensively used worldwide to control herbs, weeds, pests, and other competing agents with various growing crops. The consumption of crops grown with these chemicals (even in small quantities) can upshot into accumulation in the human body. People can accidentally inhale these hazardous chemicals if they are in an area where they were applied. These chemicals can be ingested in a human with contaminated food and drinks. Ultimately it causes various adverse effects (chronic toxicity, teratogenic, mutagenic, carcinogenic effect, reproductive, and organ toxicity) on human health. Among the pool of these chemicals used as pesticides in the environment, exposure of endosulfan to humans has a potential health risk throughout the globe. The poisoning of endosulfan is reported frequently in society, therefore, this article highlights the toxicological and other harmful properties of endosulfan to humans and emphasized its essential biomonitoring. Its quick monitoring and effective hazard evaluation are possible with multi-omics technologies and some other analytical approaches. This review summarizes the introduction and mechanism of action of endosulfan along with some other toxic chemicals used in the agriculture work, the toxicity of endosulfan in human/environment, and importantly its biomonitoring (detection of chemicals and their metabolites in a biological sample) in human because biomonitoring is often considered as the most preferred method. Biomonitoring could be easily done in human samples (blood, hair, milk, and urine) with a multi-omics approach, which is a quick, reliable, and state-of-the-art technique. 

/pdf/biomonitoring-of-endosulfan-toxicity-in-human-r8zn1vzp.pdf

Biomonitoring of endosulfan toxicity in human

Exposure to low levels of environmental contaminants, including pesticides, induces neurodevelopmental toxicity. Environmental and food contaminants can reach the brain of the fetus, affecting brain development and leading to neurological dysfunction. The pesticide endosulfan is a persistent pollutant, and significant levels still remain detectable in the environment although its use is banned in some countries. In rats, endosulfan exposure during brain development alters motor activity, coordination, learning, and memory, even several months after uptake, and does so in a sex-dependent way. However, the molecular mechanisms driving these effects have not been studied in detail. In this work, we performed a multiomics study in cerebellum from rats exposed to endosulfan during embryonic development. Pregnant rats were orally exposed to a low dose (0.5 mg/kg) of endosulfan, daily, from gestational day 7 to postnatal day 21. The progeny was evaluated for cognitive and motor functions at adulthood. Expression of messenger RNA and microRNA genes, as well as protein and metabolite levels, were measured on cerebellar samples from males and females. An integrative analysis was conducted to identify altered processes under endosulfan effect. Effects between males and females were compared. Pathways significantly altered by endosulfan exposure included the phosphatidylinositol signaling system, calcium signaling, the cGMP-PKG pathway, the inflammatory and immune system, protein processing in the endoplasmic reticulum, and GABA and taurine metabolism. Sex-dependent effects of endosulfan in the omics results that matched sex differences in cognitive and motor tests were found. These results shed light on the molecular basis of impaired neurodevelopment and contribute to the identification of new biomarkers of neurotoxicity.

A Multiomics Study To Unravel the Effects of Developmental Exposure to Endosulfan in Rats: Molecular Explanation for Sex-Dependent Effects

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A Multiomics Study To Unravel the Effects of Developmental Exposure to Endosulfan in Rats: Molecular Explanation for Sex-Dependent Effects