Deleterious effects of in vivo parameters and oxidative stress-mediated autophagy and apoptosis induction via MAPKs and AMPK signaling pathways in the ammonia-exposed marine rotifer Brachionus plicatilis

Abstract

In this study, we investigated the molecular mechanisms responsible for the physiological and behavioral consequences of ammonia exposure in the marine rotifer Brachionus plicatilis, a representative model of aquatic invertebrates. Brachionus plicatilis is particularly susceptible to ammonia, which can induce substantial increases in antioxidant enzyme activities, including those of superoxide dismutase and catalase, along with reactive oxygen species. Furthermore, the expression of mitogen-activated protein kinases (MAPKs), a critical pathway implicated in oxidative stress, was investigated using western blots to elucidate increases in the phosphorylation of p38 among MAPKs. We also identified an adverse behavioral effect of ammonia exposure in the form of a reduction in swimming speed in B. plicatilis. Following this, the activity of acetylcholinesterase and expression of 5ʹ-adenosine monophosphate-activated protein kinase (AMPK) proteins were investigated to determine the relationship between deleterious behavioral effects and molecular responses. Western blots were also used to identify autophagy and apoptosis as molecular side effects of ammonia exposure in rotifers. Increased expression of relevant biomarkers indicated that autophagy and apoptosis occurred along with increased phosphorylation of p38 and AMPK among MAPKs. This study offers a deeper understanding of the impact of ammonia on marine organisms by investigating alterations at the molecular level, as well as physiological changes and behavioral patterns of rotifers in response to varying concentrations of ammonia.