Oct 2026· Biology· Vol 15, pp. 1795· 0 citations· 51 references
TL;DR
It is demonstrated that chronic nitrite stress progressively erodes shrimp homeostasis through tissue-specific transcriptional reprogramming, forcing resource allocation toward maintenance and defense at the expense of growth, thereby providing a mechanistic basis for nitrite risk assessment and threshold management in aquaculture.
Abstract
Nitrite nitrogen is a prevalent environmental stressor in intensive shrimp aquaculture that impairs growth and health, yet its chronic effects and underlying molecular mechanisms in Penaeus monodon remain incompletely understood. To address this, we exposed juvenile P. monodon (initial body weight 2.06–2.34 g) to 0, 4, and 8 mg/L nitrite nitrogen for 30 days, measuring survival, growth performance, hepatopancreas enzyme activities (ACP, AKP, T-AOC, T-SOD), and conducting transcriptomic profiling of gill and hepatopancreas tissues. Chronic nitrite exposure significantly reduced weight gain rate from 82.98% in the control to 39.33% (4 mg/L) and 33.86% (8 mg/L), with survival declining from 58.89% to 51.11% and 38.89%, respectively. ACP activity and antioxidant capacities (T-AOC and T-SOD) were markedly suppressed, indicating impaired immune and oxidative stress defenses. Transcriptomic analysis revealed tissue-specific responses: gills primarily adjusted nitrogen/amino-acid metabolism at 4 mg/L and mitochondrial oxidative phosphorylation at 8 mg/L, whereas the hepatopancreas showed broader reprogramming involving cell junction integrity, tryptophan–kynurenine metabolism, cofactor/vitamin metabolism, lipid remodeling, cytochrome P450-mediated detoxification, and melanization-related immune pathways at higher stress. These findings demonstrate that chronic nitrite stress progressively erodes shrimp homeostasis through tissue-specific transcriptional reprogramming, forcing resource allocation toward maintenance and defense at the expense of growth, thereby providing a mechanistic basis for nitrite risk assessment and threshold management in aquaculture.
It is shown that diploid Pacific oysters initiate early protective responses to maintain normal cellular function, but these responses may become insufficient under prolonged ammonia nitrogen stress, improving understanding of the physiological and molecular mechanisms underlying ammonia toxicity in Pacific oysters.
Salinity was the principal factor influencing antioxidant status and that its interaction with ammonia produced tissue-specific responses, particularly in the hepatopancreas, indicating that salinity was the principal factor influencing antioxidant status.
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