<p>Polystyrene microplastics (PS-MPs), an emerging environmental contaminant, have attracted significant concern in recent years. This study aimed to evaluate mitochondrial oxidative damage in renal and muscular tissues of the freshwater fish <i>Anabas testudineus</i> following exposure to environmentally relevant concentrations (13.6&#xa0;mg L⁻<sup>1</sup> and 23.6&#xa0;mg L⁻<sup>1</sup>) of PS-MPs for 1, 7, and 15&#xa0;days. Exposure to PS-MPs disrupted the antioxidant defense system within the mitochondrial compartments of renal and muscle tissues, leading to increased levels of hydrogen peroxide generation and lipid peroxidation. PS-MPs exposure altered metabolic functions in the mitochondrial fractions of kidney and muscle tissues, as evidenced by elevated activities of alanine aminotransferase and aspartate aminotransferase. Besides, exposure to PS-MPs resulted in a decline of tissue-specific marker enzymes, such as acid and alkaline phosphatases, in renal tissue, indicating tissue damage. Histological examinations revealed significant tissue damage, including necrosis of renal tubules, vacuolization, glomerular degeneration, and melanomacrophage aggregation in kidney tissues. In muscle tissues, the observed damages included myolysis, vacuolar degeneration, necrosis, and atrophy of muscle fibers. These findings suggest that oxidative stress induced by PS-MPs exposure disrupts metabolic functions in mitochondrial fractions, thereby providing valuable insights into nephrotoxicity and muscular toxicity in fish.</p>

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Influence of Polystyrene Microplastics on Mitochondrial Oxidative Damage in Renal and Muscular Tissues of the Freshwater Fish

  • Moothedath Arya,
  • Kuttichira Jithila,
  • Reeha Mashirin,
  • Kumari Chidambaran Chitra

摘要

Polystyrene microplastics (PS-MPs), an emerging environmental contaminant, have attracted significant concern in recent years. This study aimed to evaluate mitochondrial oxidative damage in renal and muscular tissues of the freshwater fish Anabas testudineus following exposure to environmentally relevant concentrations (13.6 mg L⁻1 and 23.6 mg L⁻1) of PS-MPs for 1, 7, and 15 days. Exposure to PS-MPs disrupted the antioxidant defense system within the mitochondrial compartments of renal and muscle tissues, leading to increased levels of hydrogen peroxide generation and lipid peroxidation. PS-MPs exposure altered metabolic functions in the mitochondrial fractions of kidney and muscle tissues, as evidenced by elevated activities of alanine aminotransferase and aspartate aminotransferase. Besides, exposure to PS-MPs resulted in a decline of tissue-specific marker enzymes, such as acid and alkaline phosphatases, in renal tissue, indicating tissue damage. Histological examinations revealed significant tissue damage, including necrosis of renal tubules, vacuolization, glomerular degeneration, and melanomacrophage aggregation in kidney tissues. In muscle tissues, the observed damages included myolysis, vacuolar degeneration, necrosis, and atrophy of muscle fibers. These findings suggest that oxidative stress induced by PS-MPs exposure disrupts metabolic functions in mitochondrial fractions, thereby providing valuable insights into nephrotoxicity and muscular toxicity in fish.