Application of transcriptome analysis to understand the adverse effects of hydrogen peroxide exposure on brain function in common carp (Cyprinus carpio).

Environ Pollut

Key Laboratory of Freshwater Fisheries and Germplasm Resources Utilization, Ministry of Agriculture and Rural Affairs, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi, 214081, China; International Joint Research Laboratory for Fish Immunopharmacology, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi, 214081, China. Electronic address:

Published: October 2021

Hydrogen peroxide (HO), as a common disinfectant, has been extensively used in aquaculture. The toxicity of high ambient HO for gills and liver of fish has received attention from many researchers. However, whether HO exposure induced brain injury and neurotoxicity has not been reported in fish. Therefore, this study aimed to explore the potential mechanism of HO toxicity in brain of common carp via transcriptome analysis and biochemical parameter detection. The fish were exposed to 0 (control) and 1 mM of HO for 1 h per day lasting 14 days. The results showed that HO exposure caused oxidative damage in brain evidenced by decreased glutathione (GSH), total antioxidant capacity (T-AOC) and nicotinamide adenine dinucleotide (NAD) levels, and increased formation of malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG). Meanwhile, HO exposure reduced 5-hydroxytryptamine (5-HT) level, and down-regulated tryptophan hydroxylase 1 (tph1a), tph2, 5-hydroxytryptamine receptor 1A-beta (htr1ab) and htr2b expression in brain. Transcriptome analysis showed that HO exposure up-regulated 604 genes and down-regulated 1209 genes in brain. Go enrichment displayed that the differently expressed genes (DEGs) were enriched mainly in cellular process, single-organism process, metabolic process, and biological regulation in the biological process category. Further, KEGG enrichment indicated that HO exposure led to dysregulation of neurotransmitter signals including depression of glutamatergic synapse, GABAergic synapse and endocannabinoid signaling. Also, we found the alteration of three key pathways including calcium, cAMP and HIF-1 in brain after HO exposure. In conclusion, our data indicated that HO exposure induced oxidative damage and neurotoxicity, possibly related to dysregulation of neurotransmitters and calcium, cAMP and HIF-1 signaling pathways, which may adversely affect learning, memory and social responses of common carp. This study provided novel insight into biological effects and underlying mechanism of HO toxicity in aquatic animal, and contributed to proper application of HO in aquaculture.

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Source
http://dx.doi.org/10.1016/j.envpol.2021.117240DOI Listing

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