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Background <p>Saline-alkaline stress, particularly sodium bicarbonate-induced alkaline stress, can cause tissue damage and oxidative stress in aquatic animals, thereby inhibiting their growth and even threatening their survival. This has become a key factor limiting the utilization of saline-alkaline water resources. This study for the first time systematically established acute and chronic time-series gradient NaHCO₃ stress treatments, and integrated histological observation, ultrastructural examination, enzyme activity determination as well as transcriptomic and metabolomic profiling to reveal the adaptive response mechanism of <i>M. rosenbergii</i>.</p> Results <p>In this study, <i>M. rosenbergii</i> were selected as the research object to evaluate the physiological responses under acute (96&#xa0;h) and chronic (56 d) alkaline stress at NaHCO₃ concentrations of control (0.0 mmol/L), low (3.2 mmol/L, 30% LC₅₀), and high (6.4 mmol/L, 60% LC₅₀). The results indicated that during acute NaHCO₃ stress, the oxidative stress and energy metabolism-related enzyme activities fluctuated over time, reflecting adaptive response to the stress-induced damage. Chronic exposure results showed activation of a coordinated energy network—evidenced by upregulated glycolysis, accompanied by increased expression of <i>hk2</i> and <i>glut2</i>, as well as elevated activities of HK, PFK and LDH, increased TCA intermediates (succinate, fumarate), and elevated oxidative phosphorylation metabolites, enhancing ATP production. Fatty acid metabolism exhibited a dose-dependent response: synthesis was upregulated under low stress (elevated <i>fas</i>, <i>acsbgl2</i>, and palmitic acid) likely for membrane remodeling, but suppressed under high stress. Prolonged exposure induced significant oxidative damage, evidenced by increased MDA, accumulated LysoPCs, and decreased SOD activity. Concurrently, a marked increase in autolysosomes indicated autophagy activation. Notably, these physiological disruptions were accompanied by a significant, dose-dependent decline in growth performance (FAW, WGR, SGR).</p> Conclusions <p>These findings indicate that NaHCO₃ stress induces integrated physiological responses in <i>M. rosenbergii</i>, including enhanced energy metabolism, oxidative injury, and autophagic activation, providing a reference for the development and utilization of saline-alkaline water resources.</p>

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Integrated physiological responses of Macrobrachium rosenbergii to NaHCO₃ stress: growth inhibition, energy metabolism activation, oxidative injury, and autophagic response

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月16日

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  • Heng Yu,
  • Songbao Zou,
  • Mei Liu,
  • Meng Ni,
  • Xiaoshan Jiang,
  • Mingfeng Deng,
  • Julin Yuan

摘要

Background

Saline-alkaline stress, particularly sodium bicarbonate-induced alkaline stress, can cause tissue damage and oxidative stress in aquatic animals, thereby inhibiting their growth and even threatening their survival. This has become a key factor limiting the utilization of saline-alkaline water resources. This study for the first time systematically established acute and chronic time-series gradient NaHCO₃ stress treatments, and integrated histological observation, ultrastructural examination, enzyme activity determination as well as transcriptomic and metabolomic profiling to reveal the adaptive response mechanism of M. rosenbergii.

Results

In this study, M. rosenbergii were selected as the research object to evaluate the physiological responses under acute (96 h) and chronic (56 d) alkaline stress at NaHCO₃ concentrations of control (0.0 mmol/L), low (3.2 mmol/L, 30% LC₅₀), and high (6.4 mmol/L, 60% LC₅₀). The results indicated that during acute NaHCO₃ stress, the oxidative stress and energy metabolism-related enzyme activities fluctuated over time, reflecting adaptive response to the stress-induced damage. Chronic exposure results showed activation of a coordinated energy network—evidenced by upregulated glycolysis, accompanied by increased expression of hk2 and glut2, as well as elevated activities of HK, PFK and LDH, increased TCA intermediates (succinate, fumarate), and elevated oxidative phosphorylation metabolites, enhancing ATP production. Fatty acid metabolism exhibited a dose-dependent response: synthesis was upregulated under low stress (elevated fas, acsbgl2, and palmitic acid) likely for membrane remodeling, but suppressed under high stress. Prolonged exposure induced significant oxidative damage, evidenced by increased MDA, accumulated LysoPCs, and decreased SOD activity. Concurrently, a marked increase in autolysosomes indicated autophagy activation. Notably, these physiological disruptions were accompanied by a significant, dose-dependent decline in growth performance (FAW, WGR, SGR).

Conclusions

These findings indicate that NaHCO₃ stress induces integrated physiological responses in M. rosenbergii, including enhanced energy metabolism, oxidative injury, and autophagic activation, providing a reference for the development and utilization of saline-alkaline water resources.