Cold stress changes the intestinal oxidative stress-mediated MAPK pathways and lipid metabolism in Takifugu fasciatus

Fish are poikilothermic vertebrates, serving as ideal models for investigating temperature adaptation. Water temperature is a crucial environmental factor influencing fish survival. Cold stress can reduce metabolic activity and impair digestive system function in fish, subsequently compromising intestinal integrity and causing oxidative damage. The Takifugu fasciatus is a promising fish, but is sensitive to low water temperatures. However, limited research exists on the intestine of T. fasciatus in response to cold stress. In this study, we investigated the effects of cold stress on oxidative stress, the mitogen-activated protein kinase (MAPK) pathways, lipid metabolism, and their underlying molecular mechanisms in the intestine of T. fasciatus. In vivo results showed that exposure to different temperatures (25, 19, and 13 degrees C) for varying durations (0, 6, 24, and 96 h) triggered the activation of the intestinal antioxidant system and the MAPK pathways. Simultaneously, it altered lipid metabolism and promoted triglyceride (TG) deposition in the intestine of T. fasciatus. In vitro results revealed that the ultrastructure of intestinal epithelial cells was changed after incubation at 21 degrees C for 24 h, accompanied by a notable increase in the mitochondrial count. In contrast, adding the reactive oxygen species (ROS) scavenger, Nacetyl-L-cysteine (NAC), alleviated cellular damage, negatively affected MAPK pathways activation, and inhibited TG deposition induced by cold stress. Our study elucidated that the fish intestine responds to cold stress by activating the oxidative stress-mediated MAPK pathways and altering the lipid metabolism, providing new insights into the adaptive mechanisms of fish in response to cold stress.