Brain alterations in GABA, glutamate and glutamine markers after chronic atrazine exposure in the male albino rat

Chávez-Pichardo, M E; Reyes-Bravo, D. Y.; Mendoza-Trejo, M.S.; Marín-López, Alejandra Guadalupe; Giòrdano, Magda; Hernandez-Chan, Nancy G.; Domínguez-Marchan, K; Ortega-Rosales, L C; Rodríguez, Verónica

doi:10.1007/s00204-020-02806-2

Cited by 19 publications

(19 citation statements)

References 57 publications

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“…Chronic ATR exposure to 1 or 10 mg ATR/kg increased the mRNA expression of some genes of the glutamatergic and GABAergic systems involved in the production, vesiculation, reuptake, and some of its receptors in the prefrontal cortex, nucleus accumbens, striatum, hippocampus, and ventral midbrain. The increased expression of genes related to GABAergic and glutamatergic systems could be related to the hyperactivity found in rats exposed to 10 mg ATR/kg and already reported in this chronic paradigm exposure of ATR (Bardullas et al, 2011;Chavez-Pichardo et al, 2020). These results support our previous study that showed the GABAergic and glutamatergic systems as targets of the chronic ATR exposure and the susceptibility not only of the basal ganglia but other structures such as the hippocampus and the prefrontal cortex.…”

Section: Discussionsupporting

confidence: 91%

Chronic atrazine exposure increases the expression of genes associated with GABAergic and glutamatergic systems in the brain of male albino rat

et al. 2022

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The herbicide atrazine (ATR; 2-chloro-4-ethylamino-6-isopropylamino-s-triazine) is widely used to destroy grasses and broadleaf weeds in crops and some fruits. Studies in rodents have shown that acute, repeated or chronic exposure to ATR is associated with alterations in the nigrostriatal dopaminergic pathway, whereas its effects on GABAergic and glutamatergic pathways have only recently been reported. Sprague-Dawley male rats were exposed daily to 1 or 10 mg ATR/kg of BW for 13 months to evaluate the ATR effects on GABAergic and glutamatergic systems. At the end of the ATR treatment, the levels of mRNA of several genes involved in the production, vesiculation, reuptake, and receptors of GABA and Glu in the striatum (STR), nucleus accumbens (NAcc), prefrontal cortex (PFC), ventral midbrain (vMID) and hippocampus (HIPP) were evaluated by absolute qPCR. For the GABAergic genes, increased expression of GAD67 and Slc32a1 in STR and/or vMID in rats exposed to 1 and/or 10 mg ATR were detected. With regard to the expression of genes involved in the glutamatergic system, Slc17a6 and Grin1 in HIPP of rats exposed to 1 and/or 10 mg ATR, increased as was Gria1 in STR and PFC in the group exposed to 1 mg ATR. In the same fashion, Slc1a3 expression and MGLUR1 increased in STR of rats exposed to 1 and 10 mg ATR groups. The expression of the glutaminases gls (variants 1 and 2) was greater in STR, NAcc, HIPP, and PFC of rats exposed to 1 and/or 10 mg ATR. These findings show that the GABAergic and, especially glutamatergic systems are targets of ATR exposure.

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Section: Discussionsupporting

confidence: 91%

Chronic atrazine exposure increases the expression of genes associated with GABAergic and glutamatergic systems in the brain of male albino rat

et al. 2022

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“…In humans, increased risk of intrauterine growth retardation, decreased semen content, and spontaneous abortions were found in many peer-reviewed studies, as were demasculinization and hermaphrodism in frogs [ 52 , 53 , 54 , 55 , 56 ]. Different studies have been recently demonstrated that exposure to ATR induce a dopaminergic and serotonergic toxicity, an alteration in GABA, glutamate and glutamine markers and a lot of behavioral alteration [ 32 , 45 , 57 , 58 , 59 , 60 , 61 , 62 ].…”

Section: Discussionmentioning

confidence: 99%

“…ATR contamination has been linked to many different serious health issues including neurologic conditions, [ 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 ]. In particular, its well established that ATR is able to induce changes in the antioxidant response in brain of common carp, behavioral alterations and brain acetylcholinesterase deficits in zebrafish, brain alterations in GABA, glutamate and glutamine markers in the male albino rat and many others [ 29 , 30 , 31 , 32 ].…”

Section: Introductionmentioning

confidence: 99%

Atrazine Inhalation Causes Neuroinflammation, Apoptosis and Accelerating Brain Aging

Genovese

Siracusa

Fusco

et al. 2021

IJMS

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Background: exposure to environmental contaminants has been linked to an increased risk of neurological diseases and poor outcomes. Chemical name of Atrazine (ATR) is 6-chloro-N-ethyl-N′-(1-methylethyl)-1,3,5-triazine-2,4-diamine, and it is the most commonly used broad-spectrum herbicide in agricultural crops. Several studies have demonstrated that ATR has the potential to be harmful to the brain’s neuronal circuits. Until today nobody has explored the effect of ATR inhalation on young and aged mice. Methods: young and aged mice were subject to 25 mg of ATR in a vehicle made with saline and 10% of Dimethyl sulfoxide (DMSO) every day for 28 days. At the end of experiment different behavioral test were made and brain was collected. Results: exposure to ATR induced the same response in terms of behavioral alterations and motor and memory impairment in mice but in aged group was more marked. Additionally, in both young and aged mice ATR inhalations induced oxidative stress with impairment in physiological antioxidant response, lipid peroxidation, nuclear factor kappa-light-chain-enhancer of activated B cells (nf-κb) pathways activation with consequences of pro-inflammatory cytokines release and apoptosis. However, the older group was shown to be more sensitive to ATR inhalation. Conclusions: our results showed that aged mice were more susceptible compared to young mice to air pollutants exposure, put in place a minor physiologically response was seen when exposed to it.

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“…Typically, these two neurotransmitters are studied together, because they act in concert in the brain and one is a precursor to the other. One study in male albino rats did conclude that there were increases in glutamate and GABA in several areas of the brain, but not specifically in the hypothalamus after atrazine exposure at 1 or 10 mg/kg [ 99 ]. This study suggests that there may be alterations of these concentrations in other areas of the brain as well, such as the hypothalamus, and at different points during development where GABA plays a different role.…”

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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Brain alterations in GABA, glutamate and glutamine markers after chronic atrazine exposure in the male albino rat

Cited by 19 publications

References 57 publications

Chronic atrazine exposure increases the expression of genes associated with GABAergic and glutamatergic systems in the brain of male albino rat

Chronic atrazine exposure increases the expression of genes associated with GABAergic and glutamatergic systems in the brain of male albino rat

Atrazine Inhalation Causes Neuroinflammation, Apoptosis and Accelerating Brain Aging

Mechanisms of Neurotoxicity Associated with Exposure to the Herbicide Atrazine

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