Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis最新文献

Poly- and per-fluoroalkyl substances (PFAS) are a large group of synthetic compounds having a wide array of use in consumer products and industries, such as fire suppressant foam, nonstick cookware, paper, water-proof textiles, surfactants, aeronautics, and cosmetics. This widespread distribution of PFAS, their capacity to accumulate in living organisms, and their harmful effects represent a rising concern for public health. A multitude of studies have presented information on exposure to PFAS and a broad spectrum of adverse health outcomes through animal models and observational studies. Here, we have reviewed various studies that are related to PFAS toxicity on bone and brain and its underlying mechanisms. PFAS have well-established toxicological effects on bone, such as reduced osteoblastic and increased osteoclastic activity, increased activation of peroxisome proliferator activated receptor-γ (PPAR-γ), and increased expression of WNT11. With respect to brain, PFAS have been linked with autism, somnolence, sleep disturbances, glioma, Alzheimer's, decreased cognition, increased expression of Glycogen Synthase β (GSK3β). Further research is required in several areas, such as age-specific toxicological effects of PFAS, impact of various other PFAS compounds beyond perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA), and involvement of peroxisome proliferator-activated receptors in PFAS-induced toxicity. Regarding brain toxicity, extensive research in adults is required as there is currently a relative scarcity of studies in this age group when compared to the available research conducted on children and older individuals.

Luteolin and apigenin, which are abundantly present in various vegetables, fruits, and herbs, have emerged as noteworthy candidates for therapeutic applications. Traditionally recognized for their anti-inflammatory and antioxidant activities, both luteolin and apigenin have recently demonstrated the ability to inhibit cancer cell growth across multiple cancer types in vitro and in animal models. This review provides a comprehensive summary of in vivo evidence supporting the anticancer effects of luteolin and apigenin, highlighting their mechanisms of action. The review encompasses studies on their effects on liver, lung, gastric, colon, breast, pancreatic, prostate, and skin cancers in animals. We also discuss the toxicity profiles of luteolin and apigenin. Despite the encouraging preclinical results, neither luteolin nor apigenin has yet been proven to be an effective agent against cancer in clinical trials. Therefore, this review also addresses the current challenges in translating the promising anticancer effects of flavones into clinical success, emphasizing the need for further research using advanced animal models and appropriate administration routes to increase the translational value of preclinical studies. This literature review aims to enhance understanding of the anticancer and toxicological effects of luteolin and apigenin, rather than serving as a risk assessment.

Accurately evaluating chemical risk may benefit from the development of human-relevant models capable of capturing the effects of treatments that closely mimic real-world environmental and pharmaceutical exposures. Building on our previous work (Seo et al. Arch Toxicol 98:1919-1935),¹ where cytotoxicity compromised mutation detection following short-term treatments, this study investigated mutation accumulation in both 2D and 3D HepaRG cultures following 7- and 14-day exposures with relatively non-cytotoxic N-nitrosodimethylamine (NDMA) concentrations. A multi-endpoint approach was employed to assess NDMA-induced DNA damage, micronucleus formation, and mutagenesis. Seven-day NDMA treatments were not cytotoxic but produced concentration-dependent increases in DNA damage and mutations. After 14 days of exposure, the highest NDMA concentrations produced no more than 30% cytotoxicity, and induced greater mutation frequencies compared to the 7-day exposures. Overall, the mutation frequencies induced by NDMA exhibited concentration- and treatment-duration-dependent relationships in both 2D and 3D HepaRG cultures, with notably higher mutation frequencies in 3D spheroids than in 2D cultures. Quantitative analysis by benchmark concentration (BMC) modeling demonstrated lower BMC values in 3D spheroids compared to their 2D counterparts. The predominant mutation in NDMA-treated cultures was T→C transition. These findings indicate the value of extended exposure periods for conducting in vitro genotoxicity testing in HepaRG cells.

The cosmetic and personal care product (PCP) industries have bloomed in the last ten years. Many new brand names have established themselves with various lucrative advertisements, luring youths into their primary customers. Many chemicals infused into daily day-night creams or shampoo conditioners have been established as Endocrine Disrupting Chemicals (EDC). The unseen side of the coin has been flipped in this article in an attempt to relate the rising infertility issue with these products. The study aims to explore the potential adverse effects and risk assessment of the EDCs of cosmetics and personal care products, which highlights a thorough review to indicate whether chemicals such as parabens, phthalates, or UV filters are safe for reproductive physiology. EDCs may cause severe negative impacts on the reproductive systems of both males and females which include reproductive problems such as polycystic ovarian syndrome, hypospadias, cryptorchidism, ovarian cancer, endometriosis, and poor sperm quality. Despite the widespread usage and purchase of cosmetic products in the present world, little research has been conducted on the possible effects of cosmetic EDCs on health. Consequently, further in-depth research needs to be performed in this field for a better understanding of the reproductive risks caused by cosmetic EDCs.

Heavy metals are nearly everywhere in the environment, though at low concentrations. They may come to the environment through anthropologinic or natural causes. Their primary means of naturally enriching soils come from the weathering of parent materials. Nevertheless, the usage of agricultural chemicals is equally significant. Rice fields are particularly vulnerable to heavy metal pollution, which harms human health but also lowers soil fertility and agricultural production. Majority of the potentially harmful exposure that humans experience, particularly to cadmium and arsenic, comes from the plant-based foods that we consume. This article focuses on uptake mechanisms of different heavy metals in the plant system with special reference to the responsible genes, their harmful impacts on plants, human beings and overall agricultural soils. Various remedial approaches have been discussed in this article. Numerous techniques have been investigated for the removal of heavy metals from the environment like physicochemical treatment in the soil, use of microbial agents, phytoremediation approaches etc. Traditional heavy metal remediation techniques are limited by processing challenges, costs, and the production of hazardous sludge; thus, research is increasingly directed toward using microbiological agents like bacteria and fungi for the isolation and exclusion of these toxic materials from the environment. Enhancing food safety requires reducing the accumulation of detrimental substances in crops. A molecular knowledge of heavy metals accumulation pathways may allow the design of crop types with much lower harmful substance levels in food.

Humans are continually exposed to a diverse array of environmental chemicals that can damage DNA and compromise genomic integrity. Among these genotoxic agents, acetaldehyde, acrolein, aristolochic acids, and vinyl chloride are particularly concerning due to their widespread presence in industrial emissions, dietary sources, and lifestyle-related exposures such as smoking and alcohol consumption. These compounds can induce structurally distinct forms of DNA damage including bulky DNA adducts, interstrand crosslinks, and other replication-blocking lesions. While canonical DNA repair pathways serve as the primary defense against such DNA damage, some lesions persist, challenging the capacity of DNA repair systems. If not efficiently repaired, DNA lesions may disrupt replication and transcription. In many cases, translesion synthesis polymerases are recruited to bypass unrepaired lesions, introducing mutations that contribute to agent-specific mutational signatures found in cancer genomes. This review systematically examines how each of these four exogenous chemicals induces DNA damage, the DNA repair pathways responsible for removing their lesions, and the role of translesion synthesis in shaping their mutational signatures. We also highlight how three-dimensional genome organization regulates lesion susceptibility and repair, contributing to variability of mutational landscapes.

Monosodium glutamate (MSG) is a food additive that enhances the palatability of foods, thus its frequent use both domestically and industrially. Based on the dose-factor, frequency, and duration of exposure, MSG may provoke adverse health outcomes both in animals and humans. The present report aims at providing a comprehensive analysis of the scientifically proven untoward health effects of MSG. To achieve our aim, we adopted the PRISMA guidelines and checklist and searched four databases (Scopus, Web of Science, PubMed, and Google Scholar) from 2014 to 2024. Retrieved research papers were critically appraised for quality using the ARRIVE and Joanna Briggs (JB) checklists and data analysis was conducted via the narrative synthesis method. Our analysis reveals that though MSG is generally considered safe at low doses; however, high doses and repeated exposure to MSG are associated with embryotoxicity and teratogenicity, obesity, cardiotoxicity, hepatotoxicity, kidney toxicity, neurotoxicity, endothelial dysfunction, reproductive toxicities, alteration of lipid, and glucose metabolism. Thus, chronic exposure to MSG may be of human pathological importance. The findings of the present narrative synthesis provide a rationale for informed decisions on the use and labeling of this widely used food additive.

Black cohosh (Actaea racemosa L) has been utilized for centuries by Native Americans as a traditional herbal medicine. The rhizome and root extract from black cohosh (BCE) is one of the most popular herbal dietary supplements worldwide. Due to its claimed estrogen-like effects, contemporary uses of black cohosh products are primarily for alleviating menopausal and perimenopausal symptoms. However, recent studies indicate that BCE is not only ineffective for menopausal therapy, but also induces genotoxicity through an aneugenic mode of action (MoA). Adverse effects induced by BCE have been reported in humans, with many case studies documenting outcomes ranging from mild reactions to acute liver damage and even death. Consequently, concerns about the safety of BCE have emerged. There are more than 100 chemical constituents in black cohosh products, including triterpene glycosides (>40 chemicals), polyphenols (>20 chemicals), and nitrogenous compounds (>70 chemicals). Therefore, commercially available BCE products can differ markedly in composition, leading to the potential for variable bioactivities among these complex commercial products. This review presents the latest information on the toxicological effects of BCE from both in vivo and in vitro experiments and summarizes the adverse effects of BCE in human clinical trials.

The in vitro micronucleus assay is a well-known and established component of the standard genotoxicity test battery. The growing use of nanomaterials around the world along with human exposure to them has increased the need for risk assessment with regard to safety, including potential genotoxicity. The in vitro micronucleus assay is one of the most used tests for evaluating the genotoxicity of nanomaterials. This review compiles studies since 2017 that performed assessments of micronucleus formation in vitro after cellular exposure to different nanomaterials. Genotoxicity of a broad range of nanomaterials including silver, cerium, zinc, gold, nickel, cadmium, titanium, carbon, and aluminum in different cell types were reviewed. While clear trends could be seen for some nanoparticle types like silver and cerium nanoparticles, others like gold nanoparticles showed mixed results. This review highlights the usefulness and effectiveness of the micronucleus assay for studying the genotoxicity of nanomaterials, in part, and is also careful to note that standard guidelines should be followed when conducting this assay in order to generate reliable and quality-driven data.

Increasing public interest has resulted in the widespread use of non-pharmaceutical cannabidiol (CBD) products. The sales of CBD products continue to rise, accompanied by concerns regarding unsubstantiated benefits, lack of product quality control, and potential health risks. Both animal and human studies have revealed a spectrum of toxicological effects linked to the use of CBD. Adverse effects related to exposure of humans to CBD include changes in appetite, gastrointestinal discomfort, fatigue, and elevated liver aminotransferase enzymes. Animal studies reported changes in organ weight, reproduction, liver function, and the immune system. This review centers on human-derived data, including clinical studies and in vitro investigations. Animal studies are also included when human data is not available. The objective is to offer an overview of CBD-related hepatotoxicity, metabolism, and potential CBD-drug interactions, thereby providing insights into the current understanding of CBD's impact on human health. It's important to note that this review does not serve as a risk assessment but seeks to summarize available information to contribute to the broader understanding of potential toxicological effects of CBD on the liver.