Nitrite pollution in aquatic environments, often driven by human activity, can disrupt fish physiology. Nitrite is absorbed by freshwater fish through their gills, leading to internal accumulation and interference with nitric oxide (NO) signaling, redox state, and the oxygen-carrying capacity of blood. The effects of nitrite are concentration-dependent. Although moderate environmental nitrite levels have little impact on oxygen transport, they may still interfere with NO homeostasis and cellular metabolism. We report the effects of 72 h of exposure to 10 μM nitrite on adult zebrafish blood’s O2-carrying capacity and on muscle mitochondrial activity, metabolism, and redox state. The results show that this environmentally relevant but moderate concentration of nitrite leads to decreases in fish routine oxygen consumption (rMO2) and spontaneous activity, an increase in blood nitrosyl hemoglobin (HbNO), indicating increased NO production in the blood, accumulation of nitrite in muscle tissue, oxidative stress, and changes in muscle aerobic capacity linked to a rise in mitochondrial efficiency. Parallel to these effects, increases in antioxidant capacity, arginase activity, and urea and lactate levels were observed. Globally, these results are consistent with altered NO homeostasis in the fish body induced by nitrite stress.
Fasciolo et al. (2026) studied this question.