Toxicological empirical research suggests that excessive utilization of paraquat, an herbicide, shows detrimental consequences on mammalian reproductive toxicity. The current study aims to study it as a reproductive toxin on the caprine testicular cells at 4- and 6-hour exposure duration. Paraquat treatment decreased the cell viability percentage and induced histological architectural alterations such as disruption of germinal epithelium, vacuolization, and pyknotic nuclei in the testis. The differential EB/AO staining also revealed an increased incidence of apoptosis after paraquat treatment at both dosages, i.e. 10 mM and 100 mM. Paraquat also induces oxidative stress, as evident via increased Malondialdehyde levels (a byproduct of lipid peroxidation) and a decline in the antioxidant capacity (FRAP). However, co-administration of Vitamin E significantly reduced the paraquat-mediated decline in cell viability percentage, histological alterations, and apoptosis incidences and generated oxidative stress, indicating its antioxidative properties against paraquat exposure. This research concludes that Vitamin E co-administration considerably reduced the toxicity of paraquat elicited in testicles, suggesting that Vitamin E may have advantageous potential in preventing the male gonadotoxicity caused by paraquat use in agriculture.

Microplastics (MPs) are synthetic polymer particles that are generally less than 5 mm in size and have attracted heightened scrutiny due to their pervasive presence in the environment, along with their toxicological significance. Several research investigations documented its presence in humans as a profound finding in biological tissues and fluids crossing barriers, leading to oxidative and inflammatory pathways alterations associated with blood, placenta, cardiovascular, pulmonary, nephrotic, other systems, and their disorders. Given the ubiquitous utilization of microplastics across diverse sectors, it is imperative to systematically investigate and elucidate their potential toxicological effects on biological systems through rigorous and mechanistically informed research. This review will also provide the synthesis of recent mechanistic data on the toxicity that can be caused by MPs and will determine key gaps that impede efficient human health risk evaluation. A structured literature search was conducted via PubMed, Web of Science, and Scopus databases, mostly from the studies published between 2010 and 2026. The studies of exposure characteristics and biological effects were analyzed in vitro, in vivo, and in human biomonitoring, and the primary focus of the interventions includes oxidative stress, inflammation, apoptosis, hepatotoxicity, and metabolic malfunction. MPs possess various physicochemical properties, such as a low particle size, various shapes, surface area, polymer composition, and the presence of sorbed or intrinsic additives. When MPs are taken up by cells, they can induce oxidative stress via increasing ROS, eventually leading to high lipid peroxidation, mitochondrial malfunction, DNA fragmentation, and eventually cell death. MPs also cause pro-inflammatory cytokine responses, including TNF-α, IL-1β, and IL-6, altering the immune system and cell profile, leading to systemic inflammation. In aquatic and terrestrial organisms, these microplastics have a harmful impact on growth, reproduction, and behavior in a time- and dose-dependent manner. Under conditions of controlled exposure, the organ-specific toxicities that have been reported include hepatic, renal, neurological, reproductive, and cardiovascular systems. Although the fields of mechanistic knowledge are growing, there is still a substantial amount of uncertainty; there is a lack of characterization of the long-term effects of low-dose chronic exposure, the kinetics of bioaccumulation, biodegradation potential, and transgenerational effects. In addition, there are no standardized procedures for the characterization of MPs, nor the reporting of the distribution of size or exposure measurements, which limits the comparability of cross-studies and makes it difficult to assess risks quantitatively. The dynamics of interactions of MPs between co-adsorbed contaminants like heavy metals, polycyclic aromatic hydrocarbons, and endocrine-disrupting chemicals are also yet to be explored. Although all evidence available to date does indicate biologically plausible mechanisms of MP-induced toxicity, integrated research employing standardized analytical protocols, an environmentally relevant exposure model, and human epidemiological data is required to ensure that laboratory results are translated into evidence-based public health and regulatory actions. This review offers an in-depth analysis of the existing molecular understanding of MP-induced toxicity, demonstrates organism-level impacts throughout species, and establishes vital fields for future studies. In order to develop competent guidelines to minimize MP exposure and its adverse health effects, it is crucial to cover these gaps via research that incorporates toxicology and environmental science.