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Objective <p>The study aimed to evaluate the hypoxia-induced brain injury and neuroprotective effects of pyrimidine and its derivative, arylvinylpyrimidine (AVP), in the freshwater catfish, <i>Heteropneustes fossilis</i>.</p> Methods <p>Adult and healthy fish, <i>H. fossilis</i>, were exposed to varying durations (2, 4, 6, 8, 12, 16&#xa0;h) of hypoxia (2&#xa0;mg/L dissolved oxygen; DO) to find the critical threshold duration for significant brain injury. The same was assessed via TTC (2,3,5-triphenyltetrazolium chloride) staining and formazan quantification. Based on the development of TTC negative regions and fish survival, eight hours was determined as the critical exposure point. Neuroprotection with pyrimidine and AVP was studied with different experimental groups: control, hypoxia-only, positive control, pre-treatment, and post-treatment with pyrimidine or AVP. The mitigation scale was assessed using TTC staining and formazan quantification. Golgi-Cox staining used for neuronal spine morphometry.</p> Results <p>Hypoxia induced a progressive increase in TTC negative regions, with 8&#xa0;h marking a threshold for widespread brain damage and significant formazan depletion. Post-treatment with pyrimidine and AVP led to substantial recovery of mitochondrial function and a reduction in TTC-negative regions (AVP post-treatment showing the highest efficacy). Golgi-Cox staining revealed that hypoxia caused significant dendritic spine shortening and density loss. Post-treatment restored spine length and density, with AVP demonstrating superior neuroprotection. In contrast, pre-treatment showed limited protection against hypoxia induced brain injury, including reductions in neuronal length and dendritic spine integrity.</p> Conclusion <p>Pyrimidine and especially its derivative AVP exhibit neuroprotective properties against acute hypoxia-induced brain damage in <i>H. fossilis</i>. These findings highlight their therapeutic potential in mitigating environmental hypoxic stress in aquatic vertebrates and offer promising insights into hypoxia-related neuropathology.</p>

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Mitigation of hypoxia-induced brain damage by pyrimidine and its derivative in Heteropneustes fossilis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月28日

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  • Bulbul Ali,
  • Abha Mishra

摘要

Objective

The study aimed to evaluate the hypoxia-induced brain injury and neuroprotective effects of pyrimidine and its derivative, arylvinylpyrimidine (AVP), in the freshwater catfish, Heteropneustes fossilis.

Methods

Adult and healthy fish, H. fossilis, were exposed to varying durations (2, 4, 6, 8, 12, 16 h) of hypoxia (2 mg/L dissolved oxygen; DO) to find the critical threshold duration for significant brain injury. The same was assessed via TTC (2,3,5-triphenyltetrazolium chloride) staining and formazan quantification. Based on the development of TTC negative regions and fish survival, eight hours was determined as the critical exposure point. Neuroprotection with pyrimidine and AVP was studied with different experimental groups: control, hypoxia-only, positive control, pre-treatment, and post-treatment with pyrimidine or AVP. The mitigation scale was assessed using TTC staining and formazan quantification. Golgi-Cox staining used for neuronal spine morphometry.

Results

Hypoxia induced a progressive increase in TTC negative regions, with 8 h marking a threshold for widespread brain damage and significant formazan depletion. Post-treatment with pyrimidine and AVP led to substantial recovery of mitochondrial function and a reduction in TTC-negative regions (AVP post-treatment showing the highest efficacy). Golgi-Cox staining revealed that hypoxia caused significant dendritic spine shortening and density loss. Post-treatment restored spine length and density, with AVP demonstrating superior neuroprotection. In contrast, pre-treatment showed limited protection against hypoxia induced brain injury, including reductions in neuronal length and dendritic spine integrity.

Conclusion

Pyrimidine and especially its derivative AVP exhibit neuroprotective properties against acute hypoxia-induced brain damage in H. fossilis. These findings highlight their therapeutic potential in mitigating environmental hypoxic stress in aquatic vertebrates and offer promising insights into hypoxia-related neuropathology.