The intergenerational toxic effects on offspring of medaka fish Oryzias melastigma from parental benzo[a]pyrene exposure via interference of the circadian rhythm

Benzo[a]pyrene (BaP), a widely existed polycyclic aromatic hydrocarbon pollutant in aquatic environment, has toxic effects on marine animals and their generations, but the intergenerational immunotoxic mechanism underlying has not been clearly understood. In the study, the offspring of marine medaka...

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Veröffentlicht in:Environmental pollution (1987) 2020-12, Vol.267, p.115437-115437, Article 115437
Hauptverfasser: Yin, Xiaohan, Liu, Yong, Zeb, Rabia, Chen, Fangyi, Chen, Huiyun, Wang, Ke-Jian
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Liu, Yong
Zeb, Rabia
Chen, Fangyi
Chen, Huiyun
Wang, Ke-Jian
description Benzo[a]pyrene (BaP), a widely existed polycyclic aromatic hydrocarbon pollutant in aquatic environment, has toxic effects on marine animals and their generations, but the intergenerational immunotoxic mechanism underlying has not been clearly understood. In the study, the offspring of marine medaka (oryzias melastigma) which were exposed to 0.5 μg L−1 BaP suffered from circadian rhythm oscillation disorders and severe DNA damage. Many clock-associated genes like per1 were significantly modulated in offspring, both per1 and p53 were significantly inhibited that altered the progression of cell cycle and inhibited DNA repair, which possibly resulted in the increased mortality of offspring. The hypermethylation of the per1 promotor and abnormal levels of N6-methyladenosine (m6A) suggested that the underlying mechanism was probably related to the epigenetic modification. Moreover, the offspring from paternal BaP exposure had more severe DNA damage and a higher degree of hypermethylation than those from maternal exposure. F1 larvae from BaP-exposed parents were more sensitive to BaP exposure, showing that the expression of immune and metabolism-related genes were significantly up-regulated. Taken together, the parental toxicity induced by BaP could be passed to F1 generation and the mechanism underlying was probably associated with a characteristic circadian rhythm disorder. [Display omitted] •Parental BaP exposure induced circadian rhythm disorder in offspring.•Parental BaP exposure caused immune disorder in offspring through per1 and p53.•The possible mechanism was related to per1 promotor methylation and RNA methylation.•The offspring from BaP exposed males suffered more serious effects.•F1 larvae from BaP exposed parents were more sensitive to BaP. The parental toxicity induced by BaP could be passed to F1 generation and the underlying mechanism was probably associated with circadian rhythm disorder.
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In the study, the offspring of marine medaka (oryzias melastigma) which were exposed to 0.5 μg L−1 BaP suffered from circadian rhythm oscillation disorders and severe DNA damage. Many clock-associated genes like per1 were significantly modulated in offspring, both per1 and p53 were significantly inhibited that altered the progression of cell cycle and inhibited DNA repair, which possibly resulted in the increased mortality of offspring. The hypermethylation of the per1 promotor and abnormal levels of N6-methyladenosine (m6A) suggested that the underlying mechanism was probably related to the epigenetic modification. Moreover, the offspring from paternal BaP exposure had more severe DNA damage and a higher degree of hypermethylation than those from maternal exposure. F1 larvae from BaP-exposed parents were more sensitive to BaP exposure, showing that the expression of immune and metabolism-related genes were significantly up-regulated. Taken together, the parental toxicity induced by BaP could be passed to F1 generation and the mechanism underlying was probably associated with a characteristic circadian rhythm disorder. [Display omitted] •Parental BaP exposure induced circadian rhythm disorder in offspring.•Parental BaP exposure caused immune disorder in offspring through per1 and p53.•The possible mechanism was related to per1 promotor methylation and RNA methylation.•The offspring from BaP exposed males suffered more serious effects.•F1 larvae from BaP exposed parents were more sensitive to BaP. 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In the study, the offspring of marine medaka (oryzias melastigma) which were exposed to 0.5 μg L−1 BaP suffered from circadian rhythm oscillation disorders and severe DNA damage. Many clock-associated genes like per1 were significantly modulated in offspring, both per1 and p53 were significantly inhibited that altered the progression of cell cycle and inhibited DNA repair, which possibly resulted in the increased mortality of offspring. The hypermethylation of the per1 promotor and abnormal levels of N6-methyladenosine (m6A) suggested that the underlying mechanism was probably related to the epigenetic modification. Moreover, the offspring from paternal BaP exposure had more severe DNA damage and a higher degree of hypermethylation than those from maternal exposure. F1 larvae from BaP-exposed parents were more sensitive to BaP exposure, showing that the expression of immune and metabolism-related genes were significantly up-regulated. Taken together, the parental toxicity induced by BaP could be passed to F1 generation and the mechanism underlying was probably associated with a characteristic circadian rhythm disorder. [Display omitted] •Parental BaP exposure induced circadian rhythm disorder in offspring.•Parental BaP exposure caused immune disorder in offspring through per1 and p53.•The possible mechanism was related to per1 promotor methylation and RNA methylation.•The offspring from BaP exposed males suffered more serious effects.•F1 larvae from BaP exposed parents were more sensitive to BaP. 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In the study, the offspring of marine medaka (oryzias melastigma) which were exposed to 0.5 μg L−1 BaP suffered from circadian rhythm oscillation disorders and severe DNA damage. Many clock-associated genes like per1 were significantly modulated in offspring, both per1 and p53 were significantly inhibited that altered the progression of cell cycle and inhibited DNA repair, which possibly resulted in the increased mortality of offspring. The hypermethylation of the per1 promotor and abnormal levels of N6-methyladenosine (m6A) suggested that the underlying mechanism was probably related to the epigenetic modification. Moreover, the offspring from paternal BaP exposure had more severe DNA damage and a higher degree of hypermethylation than those from maternal exposure. F1 larvae from BaP-exposed parents were more sensitive to BaP exposure, showing that the expression of immune and metabolism-related genes were significantly up-regulated. Taken together, the parental toxicity induced by BaP could be passed to F1 generation and the mechanism underlying was probably associated with a characteristic circadian rhythm disorder. [Display omitted] •Parental BaP exposure induced circadian rhythm disorder in offspring.•Parental BaP exposure caused immune disorder in offspring through per1 and p53.•The possible mechanism was related to per1 promotor methylation and RNA methylation.•The offspring from BaP exposed males suffered more serious effects.•F1 larvae from BaP exposed parents were more sensitive to BaP. The parental toxicity induced by BaP could be passed to F1 generation and the underlying mechanism was probably associated with circadian rhythm disorder.</abstract><pub>Elsevier Ltd</pub><doi>10.1016/j.envpol.2020.115437</doi><tpages>1</tpages></addata></record>
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subjects Benzo[a]pyrene (BaP)
Circadian rhythm
Hypermethylation
Intergenerational immunotoxic mechanism
Oryzias melastigma
title The intergenerational toxic effects on offspring of medaka fish Oryzias melastigma from parental benzo[a]pyrene exposure via interference of the circadian rhythm
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