Rat Embryo Exposure to All-<i>Trans</i> Retinoic Acid Results in Postnatal Oxidative Damage of Respiratory Complex I in the Cerebellum

Signorile, Anna; Sardaro, Nicola; Rasmo, Domenico De; Scacco, Salvatore; Papa, Francesco; Borracci, Pietro; Carratù, Maria Rosaria; Papa, Sergio

doi:10.1124/mol.111.073353

Cited by 4 publications

(2 citation statements)

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“…It is used for acne and as an anti-ageing component in face creams [260] and is available, without prescription, on many websites. Tretinoin treatment in pregnant rats results in postnatal mitochondrial complex 1 dysfunction in the cerebellum of the offspring [261] and has also been shown to increase levels of fear and anxiety in offspring [262]. Gestational treatment also results in a delayed appearance of the cerebellar righting reflex and reduces open-field activity in the offspring.…”

Section: Cosmetic Ingredients Targeting Autism Genesmentioning

confidence: 99%

Autism genes are selectively targeted by environmental pollutants including pesticides, heavy metals, bisphenol A, phthalates and many others in food, cosmetics or household products

Carter

Blizard

2016

Neurochemistry International

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Section: Cosmetic Ingredients Targeting Autism Genesmentioning

confidence: 99%

Autism genes are selectively targeted by environmental pollutants including pesticides, heavy metals, bisphenol A, phthalates and many others in food, cosmetics or household products

Carter

Blizard

2016

Neurochemistry International

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“…It is used for acne and as an anti-ageing component in face creams [157] and is available, without prescription, on many websites. Tretinoin treatment in pregnant rats results in postnatal mitochondrial complex 1 dysfunction in the cerebellum of the offspring [158] and has also been shown to increase levels of fear and anxiety in offspring [159]. Gestational treatment also results in a delayed appearance of the cerebellar righting reflex and reduces open-field activity in the offspring.…”

Section: Cosmetic Ingredients Targeting Autism Genesmentioning

confidence: 99%

Autism genes are selectively targeted by environmental pollutants including pesticides, heavy metals, bisphenol A, phthalates and many others in food, cosmetics or household products

Carter

Blizard

2016

Preprint

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The increasing incidence of autism suggests a major environmental influence. Epidemiology has implicated many candidates and genetics many susceptibility genes. Gene/environment interactions in autism were analysed using 206 autism genes (ASG's) to interrogate ~1 million chemical/gene interactions in the comparative toxicogenomics database. Bias towards ASG's was statistically determined for each chemical. Many suspect compounds identified in epidemiology, including tetrachlorodibenzodioxin, pesticides, particulate matter, benzo(a)pyrene , heavy metals, valproate, acetaminophen, SSRI's, cocaine, bisphenol A, phthalates, polyhalogenated biphenyls, flame retardants, diesel constituents , terbutaline and oxytocin, inter alia showed a significant degree of bias towards ASG's, as did relevant endogenous agents (retinoids, sex steroids, thyroxine, melatonin, folate, dopamine, serotonin). Numerous other endocrine disruptors selectively targeted ASG's including paraquat, atrazine and other pesticides not yet studied in autism and many compounds used in 2 food, cosmetics or household products, including tretinoin, soy phytoestrogens , aspartame, titanium dioxide and sodium fluoride. Autism polymorphisms are known to influence sensitivity to some of these chemicals and these same genes play an important role in barrier function and control of respiratory cilia sweeping particulate matter from the airways. The close gene/environment relationships, for multiple suspect pollutants, suggest that the rising incidence of autism might be chemically driven by numerous environmental contaminants in a gene dependent manner. The protective dappled camouflage of the peppered moth was rendered invalid by industrial soot covering the trees, a situation reversed by clean air acts.The rising tide of neurodevelopmental and other childhood disorders linked to multiple pollutants may need a similar solution. IntroductionAccording to the Center for disease control (CDC) http://www.cdc.gov/ncbddd/autism/data.html the USA incidence of autism spectrum disorders rose 2.2 fold from 2000 to 2010 [1]. In the UK, a five-fold increase in autism in the 1990's , reached a plateau in the 2000's up to 2010 [2]. This increased prevalence is likely partly due to environmental influences, of which there are many candidates. Many chemical classes or specific chemicals related to autism have been reviewed by Rossignol and co-authors [3]. These include pesticides (chlorpyrifos, dicofol dialkylphosphate ,endosulfan, the Dichlorodiphenyltrichloroethane (DDT) metabolite o,p′dichlorodiphenyltrichloroethane, polychlorinated dibenzo-p-dioxin, polychlorinated and Polybrominated diphenyls, dichlorodiphenyldichloroethylene, heavy metals (aluminium, arsenic, cadmium, mercury, lead , nickel and manganese) , air pollutants (carbon monoxide, diesel components, methylene chloride, nitrogen dioxide, ozone, particulate matter, A number of compounds detailed above have been shown to produce autism-relevant behavioural effects in laboratory models when administered prenatally. F...

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Modulation of Benzo[a]Pyrene Induced Anxiolytic-Like Behavior by Retinoic Acid in Zebrafish: Involvement of Oxidative Stress and Antioxidant Defense System

2017

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Benzo[a]pyrene (B[a]P) is commonly associated with oxidative stress-induced neurotoxicity. Retinoic acid (RA) has been shown to exhibit neuroprotection in brain, and disruption of RA signaling via excess or deficient RA can lead to oxidative stress. B[a]P contamination in aquatic environment has been shown to lower the internal RA level. Thus, the present study was conducted in wild-type zebrafish to ameliorate the neurotoxic effect of B[a]P by waterborne RA co-supplementation. Findings showed that B[a]P induced anxiolytic-like behavioral response, and altered antioxidant activity in zebrafish is attenuated by RA. Our study also advocated the neurotoxic potential of RA treatment alone in control condition. Previous findings showed that periventricular gray zone (PGZ) of optic tectum (TeO) in zebrafish brain regulates anxiety-like behavior. The augmented pyknotic neuronal counts in PGZ following B[a]P treatment was ameliorated by RA co-supplementation. Further, presence of B[a]P in the cell milieu is known to induce oxidative stress through increase expression of cytochrome P450 1A1 (CYP1A1), an enzyme necessary for metabolic breakdown of both B[a]P and RA. Any deviation from the required concentration of RA leads to production of reactive oxygen species. Further, low availability of RA in cell milieu is known to decrease the expression of Nrf2, a transcription factor necessary for the expression of several antioxidants and antioxidant enzymes. Recent studies also showed that RA increases glutathione synthesis and exhibits neuroprotective properties in brain cells. The findings of the present study address the potential role of exogenous RA co-supplementation as a therapeutic intervention against B[a]P-induced depletion of RA, causing neurotoxicity in zebrafish.

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Rat Embryo Exposure to All-Trans Retinoic Acid Results in Postnatal Oxidative Damage of Respiratory Complex I in the Cerebellum

Cited by 4 publications

References 57 publications

Autism genes are selectively targeted by environmental pollutants including pesticides, heavy metals, bisphenol A, phthalates and many others in food, cosmetics or household products

Autism genes are selectively targeted by environmental pollutants including pesticides, heavy metals, bisphenol A, phthalates and many others in food, cosmetics or household products

Autism genes are selectively targeted by environmental pollutants including pesticides, heavy metals, bisphenol A, phthalates and many others in food, cosmetics or household products

Modulation of Benzo[a]Pyrene Induced Anxiolytic-Like Behavior by Retinoic Acid in Zebrafish: Involvement of Oxidative Stress and Antioxidant Defense System

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