Cardiac and Cerebellar Histomorphology and Inositol 1,4,5-Trisphosphate (IP3R) Perturbations in Adult Xenopus laevis Following Atrazine Exposure

Jaclyn Asouzu Johnson,Pilani Nkomozepi,Prosper Opute,Ejikeme Felix Mbajiorgu

doi:10.3390/app112110006

Jaclyn Asouzu Johnson, Pilani Nkomozepi + Show 2 more

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https://doi.org/10.3390/app112110006

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Abstract

Despite several reports on the endocrine-disrupting ability of atrazine in amphibian models, few studies have investigated atrazine toxicity in the heart and cerebellum. This study investigated the effect of atrazine on the unique Ca2+ channel-dependent receptor (Inositol 1,4,5-trisphosphate; IP3R) in the heart and the cerebellum of adult male Xenopus laevis and documented the associated histomorphology changes implicated in cardiac and cerebellar function. Sixty adult male African clawed frogs (Xenopus laevis) were exposed to atrazine (0 µg/L (control), 0.01 µg/L, 200 µg/L, and 500 µg/L) for 90 days. Thereafter, heart and cerebellar sections were processed with routine histological stains (heart) or Cresyl violet (brain), and IP3R histochemical localization was carried out on both organs. The histomorphology measurements revealed a significant decrease in the mean percentage area fraction of atrial (0.01 µg/L and 200 µg/L) and ventricular myocytes (200 µg/L) with an increased area fraction of interstitial space, while a significant decrease in Purkinje cells was observed in all atrazine groups (p < 0.008, 0.001, and 0.0001). Cardiac IP3R was successfully localized, and its mean expression was significantly increased (atrium) or decreased (cerebellum) in all atrazine-exposed groups, suggesting that atrazine may adversely impair cerebellar plasticity and optimal functioning of the heart due to possible disturbances of calcium release, and may also induce several associated cardiac and neural pathophysiologies in all atrazine concentrations, especially at 500 µg/L.

Highlights

Atrazine is designed to impair the physiology of weeds [1]; the physical and chemical properties of atrazine, such as its half-life, slow degradation [2], and solubility in different mediums, contribute to its persistence in the environment and, its contamination of ground, surface, and drinking water [3,4,5]
Groups compared to the control, while the area fraction of myocytes significantly increased in the 500 μg/L group compared to the 0.01 μg/L group
The semiquantitative waviness of the myocytes in the atrium was significantly increased in all atrazine-exposed groups compared to the control, as well as in the 0.01 μg/L group compared to the 200 μg/L

Summary

Introduction

Atrazine is designed to impair the physiology of weeds [1]; the physical and chemical properties of atrazine, such as its half-life, slow degradation [2], and solubility in different mediums, contribute to its persistence in the environment and, its contamination of ground, surface, and drinking water [3,4,5]. Atrazine and its metabolites can bio-accumulate in aquatic microbiota with adverse aquatic ecosystem implications [12] and can induce several organ toxicities in non-target organisms In organs such as the cerebellum, mostly physiological and biochemical effects of atrazine have been reported relative to perturbations of cerebellar pathophysiology and cerebral oxidative stress in quails and rats [13,14,15], as well as behavioral and neurotransmitter deficits in mice [16]. Atrazine is widely known for its ability to disrupt estrogen and androgen receptors [18], but little is known about atrazine-induced effects on the histopathology of voltage-gated receptors (IP3 Rs) in the heart (peripheral) and cerebellum (central) and the differential effects in both organs relative to their crucial functions

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