Paternal exposure to a common herbicide alters the behavior and serotonergic system of zebrafish offspring

Lamb, Simon D.; Chia, Jolyn H.Z.; Johnson, Sheri L.

doi:10.1371/journal.pone.0228357

Cited by 20 publications

(21 citation statements)

References 136 publications

(155 reference statements)

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“…This conclusion was confirmed in the novel object recognition test [ 97 ]. In zebrafish, it was also observed that paternal atrazine exposure at 0.3, 3, or 30 ppb had intergenerational dysfunction of the serotonergic system in the offspring [ 98 ]. Although only a few limited studies have been completed, each gives support that atrazine may interfere with the serotonergic system with potential for sex-specific responses at doses near or below the current chronic dietary NOAEL at 1.8 mg/kg/day.…”

Section: Effects Of Atrazine On Major Neurotransmittersmentioning

confidence: 99%

Mechanisms of Neurotoxicity Associated with Exposure to the Herbicide Atrazine

Stradtman

Freeman

2021

Toxics

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Atrazine is an herbicide commonly used on crops to prevent broadleaf weeds. Atrazine is an endocrine-disrupting chemical mainly targeting the neuroendocrine system and associated axes, especially as a reproductive toxicant through attenuation of the luteinizing hormone (LH). Current regulatory levels for chronic exposure are based on no observed adverse effect levels (NOAELs) of these LH alterations in rodent studies. Atrazine has also been studied for its effects on the central nervous system and neurotransmission. The European Union (EU) recognized the health risks of atrazine exposure as a public health concern with no way to contain contamination of drinking water. As such, the EU banned atrazine use in 2003. The United States recently reapproved atrazine’s use in the fall of 2020. Research has shown that there is a wide array of adverse health effects that are seen across multiple models, exposure times, and exposure periods leading to dysfunction in many different systems in the body with most pointing to a neuroendocrine target of toxicity. There is evidence of crosstalk between systems that can be affected by atrazine exposure, causing widespread dysfunction and leading to changes in behavior even with no direct link to the hypothalamus. The hypothetical mechanism of toxicity of atrazine endocrine disruption and neurotoxicity can therefore be described as a web of pathways that are influenced through changes occurring in each and their multiple feedback loops with further research needed to refine NOAELs for neurotoxic outcomes.

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Section: Effects Of Atrazine On Major Neurotransmittersmentioning

confidence: 99%

Mechanisms of Neurotoxicity Associated with Exposure to the Herbicide Atrazine

Stradtman

Freeman

2021

Toxics

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“…Knowing the negative infl uence of atrazine on the reproductive system, this agent was included in the list of endocrine disrupting chemicals by some organizations and countries, such as the European Community, Japan, and the United States, as it has environmental estrogenic activity with carcinogenic potential and that it can persist in the environment for long periods [16]. The mechanism underlying neuroendocrine interference caused by atrazine remains to be elucidated, but it is known to be involved in the disruption of many pathways, including the Hypothalamic-Pituitary-Gonadal (HHG) axis, monoaminergic systems in the central nervous system, changes in cyclic Adenosine Monophosphate (cAMP)-dependent signaling pathway, as well as in epigenetic mechanisms, including microRNAs and expression of DNA methyltransferases [26]. Results of a systematic literature review conducted by Wirbisky and a study was demonstrated that atrazine aff ects the HHG axis, with eff ects on the reproductive and endocrine systems in rats and with diff erences depending on the stage of life, dose, duration of exposure and strain of rats used.…”

Section: Figurementioning

confidence: 99%

“…Furthermore, a study by Lamb evaluated the eff ects on male off spring of zebrafi sh exposed to doses of 0.3, 3 or 3 Parts Per Billion (ppb) of atrazine; their fi ndings showed that endocrine and neuroendocrine disrupting chemicals can alter or interrupt some animal behaviors, especially typical reproductive behaviors, but can also lead to anxiety, aggression, and risky behavior, especially when exposure to these agents occurs early in life [26]. Thus, the scientifi c literature shows that early exposure to endocrine disruptors can permanently modify phenotypes behavior of the animal until adulthood, interfering with molecular mechanisms such as gene expression, hormone levels and neurotransmitter levels.…”

Section: Figurementioning

confidence: 99%

Integrative Review Verification of the Influence of Atrazine Exposure on Behavioral, Neurochemical and Parkinsons Disease Disorders

Pantaleon¹,

Fukushima²,

Paula³

et al. 2021

J Biomed Res Environ Sci

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Herbicides represent the largest portion of pesticides used both worldwide and in Brazil. Many of these compounds are applied on a large scale in native forests and in urban and industrial water environments, including atrazine. Due to its low cost, ability to remain active in the soil for long periods and potential effect on weed removal, atrazine ranks 5th in the ranking of most used pesticide in Brazil. Although the use of pesticides increases agricultural production, their intensive use can often cause negative effects on fauna and flora. Studies have shown that exposure to atrazine can cause various harmful effects in mammals, of both sexes, such as structural, neuroendocrine and/or behavioral changes. Considering the seriousness of the situation and the possible toxicological and pathological implications that atrazine can generate in the animal organism, the objective of this work was to carry out an integrative literature review in order to verify the scientific panorama on issues related to atrazine exposure and its impacts, mainly with regard to its toxicity on the central nervous system. To carry out this article, a bibliographic survey of scientific material obtained in the following databases was carried out: US National Library of Medicine - National Institutes of Health (PubMed), Virtual Health Library (Latin American and Caribbean Literature in Health Sciences - LILACS), Science Direct and Google® Academic, in the last 25 years. The MeSH Terms used in the search were: “Parkinson's disease”, “atrazine”, “herbicide” and “endocrine disruptor”. The following were found in the Science Direct indexers: 115 records, PubMed 52 records, in LILACS no articles were found, and 1330 records were found in Google® Academic.

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“…Progeny from five families per treatment (n=5 hypoxia, n=5 control) were generated by in vitro fertilisation (IVF) (Johnson Sheri L. et al, 2018;Lamb et al, 2020) seven days after parental exposure finished. Briefly, eggs and sperm were collected using abdominal massage -half the sperm was used for IVF and the other half was stored for subsequent DNA extraction.…”

Section: Hypoxia Tolerance Assays and Analysismentioning

confidence: 99%

“…Here we use zebrafish to further explore the phenomenon of transgenerational acclimation of hypoxia in fishes. We focus on paternal exposure as we predict that environmental specific information can be transferred via sperm, as observed in other studies (Dias and Ressler, 2013;Lamb et al, 2020;Wang et al, 2016). We test whether paternal exposure to hypoxia stimulates phenotypic responses in offspring, using behavioural phenotyping to identify resistance to acute hypoxia (time to loss of equilibrium).…”

Section: Introductionmentioning

confidence: 99%

Paternal hypoxia exposure primes offspring for increased hypoxia resistance

Ragsdale

Ortega‐Recalde

Dutoit

et al. 2020

Preprint

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In a time of rapid environmental change, understanding how the challenges experienced by one generation can influence the fitness of future generations is critically needed. Using tolerance assays, transcriptomic and methylome approaches, we use zebrafish as a model to investigate transgenerational acclimation to hypoxia. We show that short-term paternal exposure to hypoxia endows offspring with greater tolerance to acute hypoxia. We detected two hemoglobin genes that are significantly upregulated by more than 7-fold in the offspring of hypoxia exposed males. Moreover, the offspring which maintained equilibrium the longest showed greatest upregulation in hemoglobin expression. We did not detect differential methylation at any of the differentially expressed genes, suggesting that another epigenetic mechanism is responsible for alterations in gene expression. Overall, our findings suggest that a ‘memory’ of past hypoxia exposure is maintained and that this environmentally induced information is transferred to subsequent generations, pre-acclimating progeny to cope with hypoxic conditions.

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Paternal exposure to a common herbicide alters the behavior and serotonergic system of zebrafish offspring

Cited by 20 publications

References 136 publications

Mechanisms of Neurotoxicity Associated with Exposure to the Herbicide Atrazine

Mechanisms of Neurotoxicity Associated with Exposure to the Herbicide Atrazine

Integrative Review Verification of the Influence of Atrazine Exposure on Behavioral, Neurochemical and Parkinsons Disease Disorders

Paternal hypoxia exposure primes offspring for increased hypoxia resistance

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