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The interaction between polyethylene microplastics and ciprofloxacin on inducing hepatotoxicity in Carassius auratus via the gut-liver axis

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Researchers co-exposed crucian carp to polyethylene microplastics and the antibiotic ciprofloxacin and assessed liver toxicity through the gut-liver axis. The combination caused greater hepatic injury than either contaminant alone—disrupting gut microbiota, increasing intestinal permeability, and amplifying liver inflammation—highlighting synergistic toxicity when fish are exposed to both antibiotic and plastic pollution.

Polymers
Body Systems

Microplastics (MPs) can accumulate and enrich antibiotics in aquatic environments, with their interactions exacerbating threats to aquatic organisms and complicating hepatotoxicity. Therefore, this study aimed to elucidate the effects of single or combined exposure to polyethylene MPs and ciprofloxacin (CIP) on hepatic injury in crucian carp, and to reveal the potential gut-liver axis toxicity mechanisms. The results showed that MPs enhanced the bioaccumulation of CIP, which increased with increasing MPs concentration. Co-exposure induced extensive eosinophilic necrosis and localised hepatocyte clustering in hepatocytes, alongside severe vacuolization and lymphocytic infiltration in intestinal cells. Glutamate aminotransferase and alanine aminotransferase activities, and total antioxidant capacity levels in the liver were significantly elevated, whilst glutamyltransferase activities were suppressed by the co-exposure. High-concentration MPs in combination with CIP significantly enriched the pathways of amino acid metabolism, glycerophospholipid metabolism, and primary bile acid biosynthesis in the liver. Moreover, co-exposure markedly suppressed the abundance of Cetobacterium while promoting that of Gemmobacter and Bosea. The imbalances in Bacteroides and pathogens (Aeromonas and Bose) are closely associated with related products in primary bile acid biosynthesis and glycerophospholipid metabolism pathways. These findings underscore that exposure to MPs and CIP induces hepatitis and reveal the pivotal role of the indirect gut-liver axis in elucidating the potential mechanisms underlying hepatotoxicity induced by co-exposure, thereby furnishing critical evidence for the holistic assessment of health hazards posed by these pollutants.

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