ABSTRACT Selecting low‐toxicity pesticides for Integrated Pest Management (IPM) is vital to protecting non‐target natural enemies and maintaining ecosystem health. This study assessed the ecotoxicological risk and natural enemies' differential sensitivity to pesticide‐driven biodiversity threats in tropical wetland rice fields in Ndop, Cameroon. The ecotoxicological risks associated with current farming schemes of 626 farmers were assessed using the Pesticides RIsks in the Tropics to Man, Environment and Trade (PRIMET) model based on farmers' pesticide application schemes, toxicity endpoints of the most sensitive parasitic wasp ( Aphidius rhopalosiphi ) and predatory mite ( Typhlodromus pyri ) species, and pesticide physicochemical properties. Wilcoxon signed‐rank test was used to compare pesticide application concentrations and risk profiles, and pairwise ratio analysis was used for differential sensitivity analysis. Pearson correlation established relationships between variables. Approximately 76.46% of the 17 pesticides (paraquat dichloride, 2,4‐D amine, glyphosate, carbendazim, chlorothalonil, copper (I) oxide, maneb, mancozeb, metalaxyl, potassium phosphonate, acetamiprid, chlorpyrifos, cypermethrin, emamectin benzoate, fipronil, imidacloprid, lambda‐cyhalothrin) used by farmers were overused, with the PRIMET model predicting definite or possible risks to both species for all seven insecticides, and lambda‐cyhalothrin (ETR = 98 800) and cypermethrin (ETR = 122 000) posing the highest acute and chronic definite risks. The fungicides carbendazim, metalaxyl, maneb, and chlorothalonil posed a possible risk (ETR ≤ 100) to T. pyri , while mancozeb posed a definite risk (ETR = 189.7) to A. rhopalosiphi . In contrast, chlorpyrifos (ETR = 6213) and fipronil (ETR = 4463) posed the highest definite risks to A. rhopalosiphi. Overall risk levels did not differ significantly between the two species ( p < 0.9), with T. pyri sensitive to 42.9% of applied pesticides and showing 284‐fold higher differential sensitivity than A. rhopalosiphi , mostly to pyrethroids. Pearson correlation revealed a highly significant positive relationship between lethal rates and applied concentrations ( r = 0.723, p < 0.001). Farmers in wetlands should replace high‐risk pesticides, especially pyrethroids, and adopt IPM to reduce risks to non‐target beneficial arthropods.
ABSTRACT Heavy metals in the environment are known pollutants whose relevance is increasingly being recognized due to their role in the global prevalence of metabolic diseases. In fact, people are usually exposed to mixtures of various metals, such as arsenic, cadmium, lead, mercury, and others, rather than single metal compounds, which happens due to pollution of the environment, occupation, and ingestion of foods and water that contain toxins. There is evidence that suggests that these metal exposures can be more dangerous than expected from studies of single exposures, as all of them act through the same mechanisms, such as oxidative stress, inflammation, mitochondrial impairment, and disruption of endocrine balance. Thus, in this article, a systems biology approach will be utilized to understand the metabolic effects of heavy metal mixtures and assess associated risks. The combination of multiple metals is associated with more stress to the system when compared to the stress caused by exposure to a single metal. This is due to factors such as insulin resistance, toxic effect on the β cell, which secretes insulin, dyslipidemia, and type 2 diabetes development risk. Multi‐metal exposure does not only happen through different exposure routes but rather through molecular nodes common for regulating redox balance, mitochondria, inflammation, endocrine function, and epigenetics. The introduction of mixture modeling, biomarker profiling, and multi‐omics approaches based on the exposome, understanding how multi‐metal exposures influence coordinated metabolic disruption, will be enhanced. Metals in mixtures exhibit cumulative and interactive effects that traditional single‐metal risk assessment models overlook, leading to an underestimation of metabolic risk. It is, therefore, necessary to shift towards risk frameworks based on mixtures that integrate state‐of‐the‐art statistical modeling with exposomic and multi‐omics platforms. The strategy would bolster preventive environmental health approaches and improve the identification of people with greater susceptibility to environment‐driven metabolic disease.
ABSTRACT Pyriproxyfen is an aromatic, nonterpenoid, pyridine‐based hormone that acts as a juvenile regulator that mimics the equilibrium of natural juvenile hormones by blocking the development of insects into adulthood. However, it acts as an endocrine‐disrupting chemical and causes reproductive toxicity in mammals. Hence, the current study aimed to explore the harmful consequences induced by pyriproxyfen in the male Sprague Dawley rats. Twenty adult male rats were exposed to chronic doses of pyriproxyfen (62, 124, and 186 mg/kg) for 28 days. In the rats, the BMI and the blood glucose level decreased significantly after being treated with both low and high doses of pyriproxyfen. The biochemical analysis shows increased levels of antioxidant activities and metabolic biomarkers including superoxide dismutase (SOD), reactive oxygen species (ROS), catalase (CAT), total protein content, cholesterol, LDH, and triglycerides in the rats exposed to both low and high doses of pyriproxyfen. Overall cortisol concentrations differed significantly among the experimental groups, with higher mean concentrations observed in PPF‐treated groups. Sperm motility and viability were reduced following PPF exposure, while DSP showed significant reductions at the higher doses. Histopathological examination revealed disruption of seminiferous tubular architecture, increased luminal space, reduced epithelial organization, clumping of spermatozoa, and degenerative changes in the testicular tissue.
ABSTRACT The aquatic biome is exposed to a significant threat of persistent contamination by polyethylene (PE) in the ecosystem. A critical research gap exists in PE‐induced tissue‐specific bioaccumulation, associated immune and stress responses in fish, followed by potential bioremediation solutions. The present study investigated the bioaccumulation of PE particles and subsequent oxidative stress in Labeo rohita induced by two different doses (0.1 and 0.5 mg/L) over 2 weeks. Additionally, the biodegradation potential of gut‐associated microbial isolates was also evaluated. We found that PE accumulation was highest in the intestine (33.0 ± 2.5 particles/g), followed by gills (20.5 ± 1.9 particles/g) and liver (8.0 ± 1.4 particles/g), indicating a significant, dose‐ and time‐dependent increase. Substantially, it triggered a tissue‐wise oxidative stress response of antioxidant ( SOD , CAT , GPx ) and stress marker ( Hsp70 ) genes, showing significant upregulation in gill, liver, and intestine. Furthermore, this work identified a gut‐associated bacterium, Proteus vulgaris KG‐SD‐15807, demonstrating significant PE biodegradation capability. Quantitative analysis revealed achievement of 3.00% ± 0.16% weight loss over 30 days of incubation. Qualitative characterization through FT‐IR, FE‐SEM, and GC–MS analyses indicated polymer oxidation, surface erosion, and formation of distinct metabolic degradation intermediates. The present findings reveal the significant bioaccumulation and stress response due to PE in a commercially important fish, Labeo rohita . Moreover, the identified bacterium acted as a PE biodegradation agent. This research has significant implications for future explorations focused on the long‐term impacts of PE in aquatic animals and the optimization of biodegradation efficiency of Proteus vulgaris for applied bioremediation.
ABSTRACT Microplastics (MPs) are emerging environmental contaminants with increasing evidence of immunotoxic effects in invertebrates; however, their underlying cellular mechanisms remain insufficiently understood. This study investigated whether short‐term internal exposure to 1 μm polystyrene microplastics affects immune and oxidative responses in Galleria mellonella . Larvae were injected with 1, 5, 20, 40, and 80 mg/mL PS‐MPs ( n = 16 per parameter), and total hemocyte count, encapsulation and melanization responses, phenoloxidase (PO) activity, antioxidant enzymes (SOD and CAT), malondialdehyde (MDA), and total hemolymph protein levels were evaluated. Microplastic exposure significantly reduced circulating hemocyte abundance across all concentrations (control: 232.75 × 10 5 cells/mL; lowest at 1 mg/mL: 148.44 × 10 5 cells/mL). Encapsulation and melanization responses were markedly suppressed, with strong encapsulation declining from 42.49% in controls to 4.31% at 20 mg/mL, and strong melanization decreasing from 19.38% to 0.77% at 5 mg/mL. Despite the pronounced impairment of cellular immune responses, systemic PO, SOD, and CAT activities showed no robust concentration‐specific changes. In contrast, measured MDA levels decreased at ≥ 20 mg/mL, while total hemolymph protein levels increased at selected concentrations. The concurrent reduction in circulating hemocyte abundance and impairment of encapsulation and melanization indicate substantial disruption of hemocyte‐mediated cellular immune function. Because hemocyte subpopulations, particle internalization, and cell viability were not directly assessed, the present data do not identify a specific hemocyte subtype or intracellular mechanism responsible for these effects. Overall, these findings demonstrate that controlled internal PS‐MP exposure impairs cellular immune responses in G. mellonella , while systemic enzymatic responses are comparatively less affected.
