Xingkai Lake Topmouth Culter (Culter alburnus) Exhibits Biochemical and Histopathological Alterations upon Acute Ammonia Exposure

TL;DR

This study shows how acute ammonia exposure affects the liver of a fish species in Xingkai Lake, causing stress, oxidative damage, and genetic changes.

Contribution

The study provides new insights into the physiological and genetic responses of Culter alburnus to ammonia stress.

Findings

Ammonia exposure caused significant oxidative damage and physiological stress in the fish liver.

High ammonia concentrations upregulated apoptosis-related genes like P53, Bax, and Caspase-3.

Histopathological changes confirmed ammonia-induced liver damage in a concentration- and time-dependent manner.

Abstract

The Xingkai Lake topmouth culter (Culter alburnus) is an endemic, economically valuable fish in Heilongjiang that is highly sensitive to ammonia. However, the systemic effects of acute ammonia stress on its liver have not been determined. The objective of this study was to elucidate the changes in and relationships among stress biomarkers, antioxidant defense mechanisms, apoptosis indicators, and histopathological alterations in the liver of C. alburnus, a fish species native to Xingkai Lake, China, under acute ammonia exposure. Guided by the findings of a 96 h-LC50 assay, the researchers subjected the fish to 48 h of acute exposure at specified total ammonia nitrogen (TAN) concentrations of 30 mg/L, 36 mg/L, and 40 mg/L. A comprehensive assessment of physiological and biochemical markers, including cortisol (COR), blood ammonia (Amm), blood glucose (Glu), aspartate aminotransaminase (AST), alanine aminotransaminase (ALT), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA), revealed pronounced physiological stress and oxidative damage, particularly in the high-concentration groups. The physiological effects of ammonia exposure on C. alburnus showed a clear concentration and time dependence. Notably, elevated ammonia levels significantly upregulated apoptosis-associated genes such as P53, Bax, and Caspase-3. These findings were further substantiated by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assays and histopathological examinations. Overall, the study demonstrated that acute ammonia exposure exerted substantial impacts on the physiological, biochemical, and genetic expression profiles of C. alburnus in Xingkai Lake, leading to sustained stress and oxidative damage, especially at elevated concentrations (30–40 mg/L).

Figures