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.
ABSTRACT Antibiotic residues, particularly fluoroquinolones, increasingly co‐occur with salinity fluctuations in coastal areas, yet their combined effects on marine bivalves remain poorly understood. This study evaluated the interactive impact of enrofloxacin (ENR; 5 and 500 ng/L) and salinity (30 and 40 PSU) on the marine bivalve Ruditapes philippinarum , using an integrative biomarker approach to assess metabolic, oxidative, and cellular responses. Salinity emerged as the dominant factor influencing physiological patterns, as shown by multivariate analysis, with proline levels, electron transport system (ETS) activity, and lipid peroxidation (LPO) driving treatment differentiation. Exposure to high salinity alone was associated with osmotic adjustment through proline accumulation, enhanced metabolic activity, and maintenance of lipid reserves. In contrast, under combined stress (ENR at 40 PSU), clams exhibited reduced proline content, depletion of lipid reserves, and decreased ETS activity, indicating metabolic depression and reallocation of energy reserves. Under combined exposure (ENR at 40 PSU), proline accumulation decreased, lipids were depleted, and ETS activity declined, indicating metabolic depression and mobilization of energy reserves. LPO levels were lower under dual stress than under high salinity condition alone, suggesting a reduced mitochondrial reactive oxygen species production. Cellular energy allocation (CEA) further reflected increased energetic costs under combined conditions. These findings demonstrate that salinity acts as a key modulator of antibiotic toxicity, producing non‐linear and context‐dependent responses. This highlights the need to incorporate environmental variability into ecotoxicological assessments, particularly in light of climate‐driven changes in coastal salinity regimes.
ABSTRACT Lead (Pb) exposure remains an important environmental health concern because of its bioaccumulation and toxicity to multiple organs, including the liver, kidneys, and male reproductive system. This study evaluated the protective effects of a standardized Trigonella foenum‐graecum L . (fenugreek; TFG) seed extract against subchronic lead acetate‐induced toxicity in rats. An integrated experimental design assessed biochemical, oxidative, molecular, endocrine, histopathological, and sperm functional parameters. Animals were assigned to control, TFG extract (50 or 100 mg/kg), lead acetate, and combined lead plus TFG extract groups. Lead exposure caused hepatorenal dysfunction and histopathological injury, accompanied by increased malondialdehyde (MDA), reduced antioxidant defenses, increased nuclear factor kappa B (NF‐κB) protein expression, and reduced nuclear factor erythroid 2‐related factor 2 (Nrf2) and heme oxygenase‐1 (HO‐1) protein expression. Lead exposure also decreased circulating follicle‐stimulating hormone (FSH) and luteinizing hormone (LH) concentrations and impaired sperm motility, density, morphology, viability, and testicular architecture. Coadministration of the TFG extract significantly attenuated these alterations, improved biochemical and antioxidant indices, reduced NF‐κB expression, increased Nrf2 and HO‐1 expression, improved gonadotropin concentrations and sperm quality, and ameliorated hepatic and testicular histopathology. For most endpoints, the 100 mg/kg/day dose produced greater numerical improvement than 50 mg/kg/day, although between‐dose differences were not consistently significant. These findings indicate that the chemically characterized fenugreek extract attenuates lead‐induced systemic and reproductive toxicity in this preclinical rat model, with effects associated with improved redox balance, inflammation‐related protein expression, gonadotropin concentrations, and spermatogenic outcomes. Further studies are required before therapeutic or translational conclusions can be drawn.
ABSTRACT This study investigates the chronic effects of chlordecone (CLD) and propylparaben (PP), two pro‐estrogenic endocrine disruptors, on Hydra vulgaris Pallas, 1766 using a multiscale approach over a 14‐day exposure period. Environmentally relevant concentrations of CLD (0.5, 5, 20 μg L −1 ) and PP (0.01, 0.05, 0.40 μg L −1 ) were tested individually and in mixtures. CLD and PP single exposures reduced the asexual reproductive rate (RHR) by 20% at intermediate CLD and high PP concentrations, whereas mixtures caused stronger declines up to 60.0% at high concentration. Severe morphological damage occurred only under high‐dose mixtures. We analyzed the expression of 17 genes covering detoxification, oxidative stress, endocrine function, regeneration, neurotransmission, proteolysis, and epigenetic regulation. Except for G6pd and Thypedin , single exposures to CLD and PP either increased or decreased gene expression. Only a limited subset of genes ( Cyp17‐like and Cyp1a‐like under CLD; Cyp17‐like , G6pd , and Thypedin under PP) displayed dose‐related tendencies, while most other genes showed non‐monotonic or irregular responses typical of endocrine disruptors. Mixture effects included antagonism, potentiation, and coalition, with non‐monotonic responses such as Cyp17‐like induction showing a 2‐fold increase at low concentration and reversal or neutralization of oxidative‐stress markers. Mixtures also increased ubiquitin in damaged hydras exposed to high‐dose mixtures and reduced global DNA methylation (up to −43%). Together, these results highlight that mixture effects diverge markedly from single‐compound responses, show no additive effects, reinforce the importance of assessing endocrine disruptors in combination, and confirm the relevance of H. vulgaris as a sensitive model at environmental concentrations.
