Exposure to mercuric chloride induces developmental damage, oxidative stress and immunotoxicity in zebrafish embryos-larvae.
Mercury (Hg) is a widespread environmental pollutant that can produce severe negative effects on fish even at very low concentrations. However, the mechanisms underlying inorganic Hg-induced oxidative stress and immunotoxicity in the early development stage of fish still need to be clarified. In the present study, zebrafish (Danio rerio) embryos were exposed to different concentrations of Hg2+(0, 1, 4 and 16μg/L; added as mercuric chloride, HgCl2) from 2h post-fertilization (hpf) to 168hpf. Developmental parameters and total Hg accumulation were monitored during the exposure period, and antioxidant status and the mRNA expression of genes related to the innate immune system were examined at 168hpf. The results showed that increasing Hg2+concentration and time significantly increased total Hg accumulation in zebrafish embryos-larvae. Exposure to 16μg/L Hg2+caused developmental damage, including increased mortality and malformation, decreased body length, and delayed hatching period. Meanwhile, HgCl2exposure (especially in the 16μg/L Hg2+group) induced oxidative stress affecting antioxidant enzyme (CAT, GST and GPX) activities, endogenous GSH and MDA contents, as well as the mRNA levels of genes (cat1, sod1, gstr, gpx1a, nrf2, keap1, hsp70 and mt) encoding antioxidant proteins. Moreover, the transcription levels of several representative genes (il-1β, il-8, il-10, tnfα2, lyz and c3) involved in innate immunity were up-regulated by HgCl2exposure, suggesting that inorganic Hg had the potential to induce immunotoxicity. Taken together, the present study provides evidence that waterborne HgCl2exposure can induce developmental impairment, oxidative stress and immunotoxicity in the early development stage of fish, which brings insights into the toxicity mechanisms of inorganic Hg in fish.
Chongqing Key Laboratory of Animal Biology, School of Life Sciences, Chongqing Normal University, Chongqing 401331, China.
Qun-Fang
QF
Zhang
Chongqing Key Laboratory of Animal Biology, School of Life Sciences, Chongqing Normal University, Chongqing 401331, China.
Ying-Wen
YW
Li
Chongqing Key Laboratory of Animal Biology, School of Life Sciences, Chongqing Normal University, Chongqing 401331, China.
Zhi-Hao
ZH
Liu
Chongqing Key Laboratory of Animal Biology, School of Life Sciences, Chongqing Normal University, Chongqing 401331, China. Electronic address: xncql@126.com.
Qi-Liang
QL
Chen
D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D004625:Embryo, Nonmammalian / Q000187:drug effects / Q000378:metabolism; D047108:Embryonic Development / Q000187:drug effects; D005978:Glutathione / Q000378:metabolism; D007113:Immunity, Innate / Q000187:drug effects; D007814:Larva / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D008627:Mercuric Chloride / Q000633:toxicity*; D018384:Oxidative Stress / Q000187:drug effects*; D010088:Oxidoreductases / Q000235:genetics / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D014874:Water Pollutants, Chemical / Q000737:chemistry / Q000633:toxicity*; D015027:Zebrafish / Q000254:growth & development* / Q000378:metabolism; D029961:Zebrafish Proteins / Q000235:genetics / Q000378:metabolism
D000975:Antioxidants; D014874:Water Pollutants, Chemical; D029961:Zebrafish Proteins; D008315:Malondialdehyde; D008627:Mercuric Chloride; D010088:Oxidoreductases; D005978:Glutathione
Developmental damage; Immunotoxicity; Mercuric chloride exposure; Oxidative stress