Mechanism of Ammonia-Induced Brain Damage in Chinese Striped-Necked Turtle (Mauremys sinensis).

Abstract

Social advancement and heightened waste discharge have resulted in escalating ammonia pollution in aquatic ecosystems, presenting toxicity hazards to aquatic fauna, especially turtles, by impairing their neurological function. To assess the ammonia effect on turtle brains, we subjected Chinese striped-necked turtles (Mauremys sinensis) to varying ammonia concentrations (CK, control; A1, 0.790 mg/L NH3; A2, 1.418 mg/L NH3) for durations of 24 and 48 h. Our data indicate that ammonia exposure markedly elevated glutamate levels and glutamate receptor mRNA expression in turtle brains, while concurrently diminishing glutamate transporter expression. These alterations resulted in an increase in brain water content, Na⁺-K⁺-Cl^- cotransporter 1 (NKCC1), and matrix metalloproteinases. The decrease in tight junction proteins and Caveolin1 levels may lead to the rupture of the blood-brain barrier and subsequent edema. The impaired blood-brain barrier and edema led to elevated calcium levels and decreased function of certain ATPases. Gene expression associated with calcium homeostasis increased, signifying an imbalance. As the exposure time and concentration of ammonia increased, the TUNEL-stained positive cells began to appear. Taken together, increased ammonia concentrations lead to glutamate accumulation, impairing the blood-brain barrier and resulting in cerebral edema. This impairs calcium homeostasis, ultimately inducing cell death. This work provides significant insights into the toxicity of ammonia to aquatic turtles, hence augmenting our comprehension of stress physiology in these species. It underscores the necessity of safeguarding aquatic ecosystems from ammonia contamination to guarantee the health and survival of turtles and other aquatic fauna.