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Background <p>N΄-Nitrosodiethylamine (NDEA) generates hepatotoxicity and, can induce mutations and cancers. NDEA potentially induces liver fibrosis and tumors in rodents which imitates human disease. The disease model provides an opportunity to understand its mechanism and discovery of novel therapeutics. Few interesting researches documented significant roles of amino acids in health and diseases, particularly in relation to liver diseases and cancer. This study aims to explore the role of valine in recuperating liver damage induced by N’-Nitrosodiethylamine (NDEA) in rodent model.</p> Results <p>By using G*Power (version 3.1.9.7) software, statistical power was found to be 0.08 (α = 0.05) for three animals per group used in the present study. NDEA administration (i.p) generated hepatotoxicity which was marked by significant elevation in ALP, AST, ALT enzymes, blood glucose, lipid peroxides, hydroxyproline, nitrite levels and reduced activity of SOD, Mg-ATPase and FBP1 along with distorted liver architecture. Animals supplemented with valine in doses of 1.7&#xa0;g kg<sup>-1</sup> b. wt /day replenished the above investigated parameters significantly in a dose-dependent manner. Restoration of Mg<sup>2+</sup>-ATPase and FBP1 in valine supplemented animals may indicate gluconeogenesis as indirect means of energy in animals. Histological examinations revealed normal liver architecture in animals of control category while severe damage, as also revealed by % fiber score, was exhibited by rodents treated with NDEA. Notably, valine supplement reduced collagen contents and improved liver anatomy within two weeks, indicating its restorative properties.</p> Conclusion <p>These results signify valine potential to restore liver functioning and architecture via lowering oxidative stress. It is envisaged that valine may have indirect participation in energy production <i>via</i> gluconeogenesis to invigorated hepatic cells to sustain detrimental effect of NDEA. Thus, valine may be a promising candidate for therapeutic intervention against experimental liver injury.</p>

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Valine supplement recuperates N′-nitrosodiethylamine-induced liver injury in rodents via reducing oxidative stress and restoring lobular architecture

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月26日

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  • Akbar Hussain,
  • Mohd Danish,
  • Riaz Ahmad

摘要

Background

N΄-Nitrosodiethylamine (NDEA) generates hepatotoxicity and, can induce mutations and cancers. NDEA potentially induces liver fibrosis and tumors in rodents which imitates human disease. The disease model provides an opportunity to understand its mechanism and discovery of novel therapeutics. Few interesting researches documented significant roles of amino acids in health and diseases, particularly in relation to liver diseases and cancer. This study aims to explore the role of valine in recuperating liver damage induced by N’-Nitrosodiethylamine (NDEA) in rodent model.

Results

By using G*Power (version 3.1.9.7) software, statistical power was found to be 0.08 (α = 0.05) for three animals per group used in the present study. NDEA administration (i.p) generated hepatotoxicity which was marked by significant elevation in ALP, AST, ALT enzymes, blood glucose, lipid peroxides, hydroxyproline, nitrite levels and reduced activity of SOD, Mg-ATPase and FBP1 along with distorted liver architecture. Animals supplemented with valine in doses of 1.7 g kg-1 b. wt /day replenished the above investigated parameters significantly in a dose-dependent manner. Restoration of Mg2+-ATPase and FBP1 in valine supplemented animals may indicate gluconeogenesis as indirect means of energy in animals. Histological examinations revealed normal liver architecture in animals of control category while severe damage, as also revealed by % fiber score, was exhibited by rodents treated with NDEA. Notably, valine supplement reduced collagen contents and improved liver anatomy within two weeks, indicating its restorative properties.

Conclusion

These results signify valine potential to restore liver functioning and architecture via lowering oxidative stress. It is envisaged that valine may have indirect participation in energy production via gluconeogenesis to invigorated hepatic cells to sustain detrimental effect of NDEA. Thus, valine may be a promising candidate for therapeutic intervention against experimental liver injury.