Transgenerational endocrine disruption and neurotoxicity in zebrafish larvae after parental exposure to binary mixtures of decabromodiphenyl ether (BDE-209) and lead

Chen, Lianguo; Wang, Xianfeng; Zhang, Xiaohua; Lam, Paul K.S.; Guo, Yongyong; Lam, James C.W.; Zhou, Bingsheng

doi:10.1016/j.envpol.2017.06.053

Cited by 64 publications

(24 citation statements)

References 63 publications

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“…The association between plasma and intraovarian/egg hormone levels in fish has not been fully elucidated, but if we assume that there is some correlation between intraovarian and circulating TH levels (Ayson and Lam 1993;Brown et al 1988;Kang and Chang 2004;Raine and Leatherland 2003), our results are in parallel with those of common carp (see above). Interestingly, our hormone measurements of the two forms (T3 higher than T4) were contrasting compared to whole body measurements in the same species (T3 lower than T4, Gardell et al 2017), and egg measurements on other species (T3 lower than T4, Chen et al 2017). We can speculate that this may be due to differential deposition of the two forms, or deiodinase function, converting T4 to T3 in the ovaries in these species and sample type.…”

Section: Discussioncontrasting

confidence: 69%

“…If egg TH levels are correlated with plasma TH levels of the mother (Kang and Chang 2004;Raine and Leatherland 2003), then any environmentallyinduced variation or thyroid disruption in the maternal circulation may influence offspring development via altering maternally-transferred hormone levels (also called transgenerational/ maternal endocrine disruption, e.g. Ruuskanen et al 2019;Chen et al 2017).…”

Section: Introductionmentioning

confidence: 99%

“…The authors suggested that this may be due to higher temperatures in Tampa Bay, and speculated that egg THs might explain the faster growth rates and metabolic rates at this site. In the rare examples on endocrine disruption, maternal experimental exposure to pollutants (lead, polybrominated diphenyl ethers and bisphenol A) resulted in decreases plasma and egg THs in zebrafish (Danio rerio) (Chen et al 2017), with delayed larvae development (Wei et al 2018). The effects of other pollutants, such as copper, on egg hormone transfer have not been addressed, yet the effects of pollutants on plasma levels (see above) suggest that such effects may be likely.…”

Section: Introductionmentioning

confidence: 99%

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Experimental copper exposure, but not heat stress, leads to elevated intraovarian thyroid hormone levels in three-spined sticklebacks (Gasterosteus aculeatus)

2020

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Climate change and pollution are some of the greatest anthropogenic threats to wild animals. Transgenerational plasticity—when parental exposure to environmental stress leads to changes in offspring phenotype—has been highlighted as a potential mechanism to respond to various environmental and anthropogenic changes across taxa. Transgenerational effects may be mediated via multiple mechanisms, such as transfer of maternal hormones to eggs/foetus. However, sources of variation in hormone transfer are poorly understood in fish, and thus the first step is to characterise whether environmental challenges alter transfer of maternal hormones to eggs. To this end, we explored the population variation and environmental variation (in response to temperature and endocrine disrupting copper) in maternal thyroid hormone (TH), transfer to offspring in a common fish model species, the three-spined stickleback (Gasterosteus aculeatus) using multiple approaches: (i) We compared ovarian TH levels among six populations across a wide geographical range in the Baltic Sea, including two populations at high water temperature areas (discharge water areas of nuclear power plants) and we experimentally exposed fish to (ii) environmentally relevant heat stress and (iii) copper for 7 days. We found that populations did not differ in intraovarian TH levels, and short-term heat stress did not influence intraovarian TH levels. However, copper exposure increased both T4 and T3 levels in ovaries. The next step would be to evaluate if such alterations would lead to changes in offspring phenotype.

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Section: Discussioncontrasting

confidence: 69%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Experimental copper exposure, but not heat stress, leads to elevated intraovarian thyroid hormone levels in three-spined sticklebacks (Gasterosteus aculeatus)

2020

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“…For example, transgenerational exposure to Pb induced its lethality on the offspring of D. magna [34]. The parental co-exposure to PBDEs and Pb enhanced developmental neurotoxicity in offspring of zebrafish [12]. The transgenerational studies urged special attentions on the long-term impacts of environmental pollutants.…”

Section: Transgenerational Effects Between Individual and Sequential mentioning

confidence: 99%

“…For example, the co-exposure of PBDEs and Pb disrupted reproduction and thyroid endocrine function in zebrafish adults with subsequent influences on the hormones in the eggs [12]. Moreover, effects of the co-exposure on the offspring showed different reproductive outcomes from individual exposure and resulted in transgenerational neurobehavioral deficits in the offspring [12]. Yet, the exposure reality is more complicated than such co-exposure effects.…”

mentioning

confidence: 99%

Transgenerational effects of different sequential exposure to 2,2′,4,4′-tetra-brominated diphenyl ether (BDE47) and lead (Pb) on Caenorhabditis elegans

Zhang

2020

Environ Sci Eur

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Background: Poly-brominated diphenyl ethers (PBDEs) and heavy metals are persistent pollutants in Yangtze River basin, China and also around the globe. In the exposure reality, they may have sequential exposures and long-term outcomes. Yet, the effects combining these two aspects remained largely unexplored. At present, the effects of 2,2′,4,4′-tetra-brominated diphenyl ether (BDE47) and lead (Pb) on Caenorhabditis elegans were studied with two sequential arrangements. One was first exposure to BDE47 and then to Pb (or vice versa) in one generation, and the other one was an early exposure to BDE47 in the parent generation (F0) and then a later exposure to Pb in the offspring (F1) (or vice versa). Results: On growth, sequential Pb-BDE47 exposure caused inhibition in exposure but stimulation in recovery, showing similarity to individual Pb results. Meanwhile, the opposite sequential BDE47-Pb exposure showed inhibition in both exposure and recovery, similar to those of individual BDE47 results. On behavior, the effects of sequential exposure were significantly different from individual results without any similarity. In transgenerational effects, F0 Pb exposure with F1 BDE47 exposure (Pb-F1-BDE47) inhibited growth, similar to the transgenerational results of individual Pb exposure. Meanwhile, the recovery effects were similar to the transgenerational results of individual BDE47. At the same time, Pb-F1-BDE47 exposure significantly hindered the recovery of behavior while the opposite BDE47-F1-Pb exposure resulted in different results. The behavioral effects in F1 showed negative correlation with the contents of γ-aminobutyric acid (GABA), while those in F1 were positively correlated with the activities of acetylcholine esterase (AChE). Conclusions: Sequential exposure to BDE47 and Pb within one generation or over generations showed significant different effects from individual results. Further studies are still needed to investigate the toxicity patterns and underlying mechanisms.

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Role of autonomic nervous system in BDE‐209 maternal exposure induced immunotoxicity in female offspring

Mao,

Tang,

et al. 2024

Environmental Toxicology

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Decabrominated diphenyl ether (BDE‐209) is a typical persistent organic pollutant that can cross the placental barrier, increasing the exposure risk for offspring. Norepinephrine (NE) from nerve terminals and acetylcholine (Ach) can bind to specific receptors on immune cells, inhibit the immune function of the body then cause immunotoxicity. However, whether maternal exposure to BDE‐209 could lead to immunotoxicity in the offspring by acting on the sympathetic and parasympathetic nervous systems remains unclear. In view of this, the pregnancy and lactation rat BDE‐209 exposure model was established and the results demonstrated that pregnancy and lactation BDE‐209 exposure could induce immunotoxicity to female offspring via affecting immunopathology (hematological and biochemical parameters, organ indices, and spleen histopathological), decreasing humoral immunity (serum hemolysin, immunoglobulins, and cytokine productions), damaging cellular immunity (splenic lymphocytes and spleen cytokine productions), and restraining nonspecific immunity. Moreover, a dramatically significant correlation was observed between spleen nerve indices and immunity indices. Additionally, the mechanism revealed that maternal BDE‐209 exposure caused offspring immunotoxicity through (1) activating MHC/PKCθ/NF‐κB pathway; (2) promoting sympathetic nervous pathway, by upregulating the expression of β2AR protein, which in turn elevating cAMP, following activate PKA and phosphorylate CREB, ultimately leading to immunotoxicity;(3) activating parasympathetic nerve pathway by reducing the binding with Ach and α7nAchR, upregulating the expression of JAK2 and phosphorylating STAT3, induced immunotoxicity of female offspring.

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Transgenerational endocrine disruption and neurotoxicity in zebrafish larvae after parental exposure to binary mixtures of decabromodiphenyl ether (BDE-209) and lead

Cited by 64 publications

References 63 publications

Experimental copper exposure, but not heat stress, leads to elevated intraovarian thyroid hormone levels in three-spined sticklebacks (Gasterosteus aculeatus)

Experimental copper exposure, but not heat stress, leads to elevated intraovarian thyroid hormone levels in three-spined sticklebacks (Gasterosteus aculeatus)

Transgenerational effects of different sequential exposure to 2,2′,4,4′-tetra-brominated diphenyl ether (BDE47) and lead (Pb) on Caenorhabditis elegans

Role of autonomic nervous system in BDE‐209 maternal exposure induced immunotoxicity in female offspring

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