Monobutyl phthalate (MBP) induces energy metabolism disturbances in the gills of adult zebrafish (Danio rerio)

Monobutyl phthalate (MBP) is a primary metabolite of an environmental endocrine disruptor dibutyl phthalate (DBP), which poses a potential threat to living organisms. In this research, the acute toxicity of MBP on energy metabolism in zebrafish gills was studied. Transmission electron microscopy (TEM) results show that 10 mg L−1 MBP can induce mitochondrial structural damage of chloride cells after 96 h of continuous exposure. The activity of ion ATPase and the expression level of oxidative phosphorylation-related genes suggest that MBP interferes with ATP synthesis and ion transport. Further leading to a decrease in mitochondrial membrane potential (MMP) and cell viability, thereby mediating early-stage cell apoptosis. Through a comprehensive analysis of principal component analysis (PCA) and integrated biomarker response (IBR) scores, atp5a1, a subunit of mitochondrial ATP synthase, is mainly inhibited by MBP, followed by genes encoding ion ATPase (atp1b2 and atp2b1). Importantly, MBP inhibits aerobic metabolism by inhibiting the key enzyme malate dehydrogenase (MDH) in the TCA cycle, forcing zebrafish to maintain ATP supply by enhancing anaerobic metabolism. [Display omitted] •MBP induced obvious gill cells lesions and early cell apoptosis in zebrafish.•MBP mainly inhibits the gene expression of ATP synthase, then ion ATPases.•MBP forces zebrafish to strengthen anaerobic metabolism to maintain ATP supply.•The decreased MDH activity is the key to the abnormal gill energy metabolism.