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Reproductive Toxicology (Elmsford, N.Y.) Aug 2018Known endocrine disruptor bisphenol A (BPA) has been shown to be a reproductive toxicant in animal models. Its structural analogs: bisphenol S (BPS), bisphenol F (BPF),... (Review)
Review
Known endocrine disruptor bisphenol A (BPA) has been shown to be a reproductive toxicant in animal models. Its structural analogs: bisphenol S (BPS), bisphenol F (BPF), bisphenol AF (BPAF), and tetrabromobisphenol A (TBBPA) are increasingly being used in consumer products. However, these analogs may exert similar adverse effects on the reproductive system, and their toxicological data are still limited. This mini-review examined studies on both BPA and BPA analog exposure and reproductive toxicity. It outlines the current state of knowledge on human exposure, toxicokinetics, endocrine activities, and reproductive toxicities of BPA and its analogs. BPA analogs showed similar endocrine potencies when compared to BPA, and emerging data suggest they may pose threats as reproductive hazards in animal models. While evidence based on epidemiological studies is still weak, we have utilized current studies to highlight knowledge gaps and research needs for future risk assessments.
Topics: Animals; Benzhydryl Compounds; Endocrine Disruptors; Female; Humans; Male; Phenols; Reproductive Health
PubMed: 29925041
DOI: 10.1016/j.reprotox.2018.06.005 -
Toxics Oct 2022Large amounts of enriched cadmium (Cd) in the environment seriously threatens the healthy and sustainable development of the aquaculture industry and greatly restricts... (Review)
Review
Large amounts of enriched cadmium (Cd) in the environment seriously threatens the healthy and sustainable development of the aquaculture industry and greatly restricts the development of the food processing industry. Studying the distribution and toxic effects of Cd in fish, as well as the possible toxic effects of Cd on the human body, is very significant. A large number of studies have shown that the accumulation and distribution of Cd in fish are biologically specific, cause tissue differences, and seriously damage the integrity of tissue structure and function, the antioxidant defense system, the reproductive regulation system, and the immune system. The physiological, biochemical, enzyme, molecular, and gene expression levels change with different concentrations and times of Cd exposure, and these changes are closely related to the target sites of Cd action and tissues in fish. Therefore, the toxic effects of Cd on fish occur with multiple tissues, systems, and levels.
PubMed: 36287901
DOI: 10.3390/toxics10100622 -
Environment International Feb 2017Insecticides are by design toxic. They must be toxic to effectively kill target species of insects. Unfortunately, they also have off-target toxic effects that can harm... (Review)
Review
Insecticides are by design toxic. They must be toxic to effectively kill target species of insects. Unfortunately, they also have off-target toxic effects that can harm other species, including humans. Developmental neurotoxicity is one of the most prominent off-target toxic risks of insecticides. Over the past seven decades several classes of insecticides have been developed, each with their own mechanisms of effect and toxic side effects. This review covers the developmental neurotoxicity of the succeeding generations of insecticides including organochlorines, organophosphates, pyrethroids, carbamates and neonicotinoids. The goal of new insecticide development is to more effectively kill target species with fewer toxic side effects on non-target species. From the experience with the developmental neurotoxicity caused by the generations of insecticides developed in the past advice is offered how to proceed with future insecticide development to decrease neurotoxic risk.
Topics: Animals; Humans; Insecticides; Nervous System; Neurotoxins; Organophosphates; Pyrethrins
PubMed: 27908457
DOI: 10.1016/j.envint.2016.11.019 -
Toxics Jan 2022The presence of toxic substances is one of the major causes of degradation of soil quality. Wildfires, besides affecting various chemical, physical, and biological soil... (Review)
Review
The presence of toxic substances is one of the major causes of degradation of soil quality. Wildfires, besides affecting various chemical, physical, and biological soil properties, produce a mixture of potentially toxic substances which can reach the soil and water bodies and cause harm to these media. This review intends to summarise the current knowledge on the generation by wildfires of potentially toxic substances, their effects on soil organisms, and other associated risks, addressing the effects of fire on metal mobilisation, the pyrolytic production of potentially toxic compounds, and the detoxifying effect of charcoal. Numerous studies ascertained inhibitory effects of ash on seed germination and seedling growth as well as its toxicity to soil and aquatic organisms. Abundant publications addressed the mobilisation of heavy metals and trace elements by fire, including analyses of total concentrations, speciation, availability, and risk of exportation to water bodies. Many publications studied the presence of polycyclic aromatic hydrocarbons (PAH) and other organic pollutants in soils after fire, their composition, decline over time, the risk of contamination of surface and ground waters, and their toxicity to plants, soil, and water organisms. Finally, the review addresses the possible detoxifying role of charcoal in soils affected by fire.
PubMed: 35051073
DOI: 10.3390/toxics10010031 -
Biology of Reproduction Apr 2021Oocyte mitochondria are unique organelles that establish a founder population in primordial germ cells (PGCs). As the oocyte matures in the postnatal mammalian ovary... (Review)
Review
Oocyte mitochondria are unique organelles that establish a founder population in primordial germ cells (PGCs). As the oocyte matures in the postnatal mammalian ovary during folliculogenesis it increases exponentially in volume, and the oocyte mitochondria population proliferates to about 100 000 mitochondria per healthy, mature murine oocyte. The health of the mature oocyte and subsequent embryo is highly dependent on the oocyte mitochondria. Mitochondria are especially sensitive to toxic insults, as they are a major source of reactive oxygen species (ROS), they contain their own DNA (mtDNA) that is unprotected by histone proteins, they contain the electron transport chain that uses electron donors, including oxygen, to generate ATP, and they are important sensors for overall cellular stress. Here we review the effects that toxic insults including chemotherapeutics, toxic metals, plasticizers, pesticides, polycyclic aromatic hydrocarbons (PAHs), and ionizing radiation can have on oocyte mitochondria. This is very clearly a burgeoning field, as our understanding of oocyte mitochondria and metabolism is still relatively new, and we contend much more research is needed to understand the detrimental impacts of exposure to toxicants on oocyte mitochondria. Developing this field further can benefit our understanding of assisted reproductive technologies and the developmental origins of health and disease (DOHaD).
Topics: Animals; Antineoplastic Agents; DNA, Mitochondrial; Drug-Related Side Effects and Adverse Reactions; Environmental Pollutants; Female; Humans; Mammals; Mitochondria; Oocytes; Oogenesis; Oxidative Stress; Pharmaceutical Preparations
PubMed: 33412584
DOI: 10.1093/biolre/ioab002 -
Current Opinion in Biotechnology Jun 2017Man-made xenobiotics, whose potential toxicological effects are not fully understood, are oversaturating the already-contaminated environment. Due to the rate of... (Review)
Review
Man-made xenobiotics, whose potential toxicological effects are not fully understood, are oversaturating the already-contaminated environment. Due to the rate of toxicant accumulation, unmanaged disposal, and unknown adverse effects to the environment and the human population, there is a crucial need to screen for environmental toxicants. Animal models and in vitro models are ineffective models in predicting in vivo responses due to inter-species difference and/or lack of physiologically-relevant 3D tissue environment. Such conventional screening assays possess limitations that prevent dynamic understanding of toxicants and their metabolites produced in the human body. Organ-on-a-chip systems can recapitulate in vivo like environment and subsequently in vivo like responses generating a realistic mock-up of human organs of interest, which can potentially provide human physiology-relevant models for studying environmental toxicology. Feasibility, tunability, and low-maintenance features of organ-on-chips can also make possible to construct an interconnected network of multiple-organs-on-chip toward a realistic human-on-a-chip system. Such interconnected organ-on-a-chip network can be efficiently utilized for toxicological studies by enabling the study of metabolism, collective response, and fate of toxicants through its journey in the human body. Further advancements can address the challenges of this technology, which potentiates high predictive power for environmental toxicology studies.
Topics: Animals; Ecotoxicology; Environmental Pollutants; Humans; Manufactured Materials; Microfluidics; Models, Animal; Models, Biological; Xenobiotics
PubMed: 28088094
DOI: 10.1016/j.copbio.2016.11.019 -
Ecotoxicology and Environmental Safety Sep 2022Parkinson's disease (PD) is a neurodegenerative disorder which mainly targets motor symptoms such as tremor, rigidity, bradykinesia and postural instability. The... (Review)
Review
Parkinson's disease (PD) is a neurodegenerative disorder which mainly targets motor symptoms such as tremor, rigidity, bradykinesia and postural instability. The physiological changes occur due to dopamine depletion in basal ganglia region of the brain. PD aetiology is not yet elucidated clearly but genetic and environmental factors play a prominent role in disease occurrence. Despite of various environmental factors, pesticides exposure has been convicted as major candidate in PD pathogenesis. Among various pesticides 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been widely investigated in PD following with paraquat (PQ), maneb (MB), organochlorines (OC) and rotenone. Effect of these pesticides has been suggested to be involved in oxidative stress, alterations in dopamine transporters, mitochondrial dysfunction, α-synuclein (αSyn) fibrillation, and neuroinflammation in PD. The present review discusses the influence of pesticides in neurodegeneration and its related epidemiological studies conducted in PD. Furthermore, we have deliberated the common pesticides involved in PD and its associated genetic alterations and the probable mechanism of them behind PD pathogenesis. Hence, we conclude that pesticides play a prominent role in PD pathogenesis and advance research is needed to investigate the alterations in genetic and mechanistic aspects of PD.
Topics: Dopamine; Humans; Maneb; Neurotoxicity Syndromes; Paraquat; Parkinson Disease; Pesticides
PubMed: 36029574
DOI: 10.1016/j.ecoenv.2022.113972 -
Toxicology Apr 2019Electron-deficient chemicals (electrophiles) react with compounds that have one or more unshared valence electron pairs (nucleophiles). The resulting covalent reactions... (Review)
Review
Electron-deficient chemicals (electrophiles) react with compounds that have one or more unshared valence electron pairs (nucleophiles). The resulting covalent reactions between electrophiles and nucleophiles (e.g., Michael addition, S2 reactions) are important, not only to Organic Chemistry, but also to the fields of Molecular Biology and Toxicology. Specifically, covalent bond formation is the operational basis of many critically important cellular processes; e.g., enzyme function, neurotransmitter release, and membrane-vesicle fusion. Given this context it is understandable that these reactions are also relevant to Toxicology, since a significant number of xenobiotic chemicals are toxic electrophiles that can react with endogenous nucleophilic residues. Therefore, the purpose of this Review is to discuss electrophile-nucleophile chemistry as it pertains to cell injury and resulting organ toxicity. Our discussion will involve an introduction to the Hard and Soft, Acids and Bases (HSAB) theory of Pearson. The HSAB concept provides a framework for calculation of quantum chemical parameters that classify the electrophile and nucleophile covalent components according to their respective electronic nature (softness/hardness) and reactivity (electrophilicity/nucleophilicity). The calculated quantum indices in conjunction with corroborative in vivo, in chemico (cell free) and in vitro research can offer an illuminating approach to mechanistic discovery. Accordingly, we will provide examples that demonstrate how this approach has been used to discern mechanisms and sites of electrophile action.
Topics: Animals; Cell Death; Environmental Exposure; Environmental Pollutants; Hardness; Humans; Models, Biological; Models, Molecular; Molecular Conformation; Risk Assessment; Structure-Activity Relationship; Xenobiotics
PubMed: 30826385
DOI: 10.1016/j.tox.2019.02.005 -
Neurochemical Research Jun 2017Human disease commonly manifests as a result of complex genetic and environmental interactions. In the case of neurodegenerative diseases, such as Parkinson's disease... (Review)
Review
Human disease commonly manifests as a result of complex genetic and environmental interactions. In the case of neurodegenerative diseases, such as Parkinson's disease (PD), understanding how environmental exposures collude with genetic polymorphisms in the central nervous system to cause dysfunction is critical in order to develop better treatment strategies, therapies, and a more cohesive paradigm for future research. The intersection of genetics and the environment in disease etiology is particularly relevant in the context of their shared pathophysiological mechanisms. This review offers an integrated view of disease-toxicant interactions in PD. Particular attention is dedicated to how mutations in the genes SNCA, parkin, leucine-rich repeat kinase 2 (LRRK2) and DJ-1, as well as dysfunction of the ubiquitin proteasome system, may contribute to PD and how exposure to heavy metals, pesticides and illicit drugs may further the consequences of these mutations to exacerbate PD and PD-like disorders. Although the toxic effects induced by exposure to these environmental factors may not be the primary causes of PD, their mechanisms of action are critical for our current understanding of the neuropathologies driving PD. Elucidating how environment and genetics collude to cause pathogenesis of PD will facilitate the development of more effective treatments for the disease. Additionally, we discuss the neuroprotection exerted by estrogen and other compounds that may prevent PD and provide an overview of current treatment strategies and therapies.
Topics: Animals; Gene-Environment Interaction; Genetic Predisposition to Disease; Humans; Metals, Heavy; Parkinson Disease; Parkinson Disease, Secondary; Pesticides
PubMed: 27613618
DOI: 10.1007/s11064-016-2052-4 -
Toxics Feb 2021Environmental problems have always received immense attention from scientists. Toxicants pollution is a critical environmental concern that has posed serious threats to... (Review)
Review
Environmental problems have always received immense attention from scientists. Toxicants pollution is a critical environmental concern that has posed serious threats to human health and agricultural production. Heavy metals and pesticides are top of the list of environmental toxicants endangering nature. This review focuses on the toxic effect of heavy metals (cadmium (Cd), lead (Pb), copper (Cu), and zinc (Zn)) and pesticides (insecticides, herbicides, and fungicides) adversely influencing the agricultural ecosystem (plant and soil) and human health. Furthermore, heavy metals accumulation and pesticide residues in soils and plants have been discussed in detail. In addition, the characteristics of contaminated soil and plant physiological parameters have been reviewed. Moreover, human diseases caused by exposure to heavy metals and pesticides were also reported. The bioaccumulation, mechanism of action, and transmission pathways of both heavy metals and pesticides are emphasized. In addition, the bioavailability in soil and plant uptake of these contaminants has also been considered. Meanwhile, the synergistic and antagonistic interactions between heavy metals and pesticides and their combined toxic effects have been discussed. Previous relevant studies are included to cover all aspects of this review. The information in this review provides deep insights into the understanding of environmental toxicants and their hazardous effects.
PubMed: 33668829
DOI: 10.3390/toxics9030042