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Malathion exposure during juvenile and peripubertal periods downregulate androgen receptor and 17-ß-HSD testicular gene expression and compromised sperm quality in rats

Published online by Cambridge University Press:  07 November 2022

Rafaela Pires Erthal*
Affiliation:
Department of General Biology, Biological Sciences Center, State University of Londrina – UEL, Rodovia Celso Garcia Cid, Londrina, Paraná 86057-970, Brazil Department of General Pathology, Biological Sciences Center, State University of Londrina – UEL, Rodovia Celso Garcia Cid, Londrina, Paraná 86057-970, Brazil
Gláucia Eloisa Munhoz de Lion Siervo
Affiliation:
Department of General Biology, Biological Sciences Center, State University of Londrina – UEL, Rodovia Celso Garcia Cid, Londrina, Paraná 86057-970, Brazil Department of General Pathology, Biological Sciences Center, State University of Londrina – UEL, Rodovia Celso Garcia Cid, Londrina, Paraná 86057-970, Brazil
Giovanna Fachetti Frigoli
Affiliation:
Department of General Biology, Biological Sciences Center, State University of Londrina – UEL, Rodovia Celso Garcia Cid, Londrina, Paraná 86057-970, Brazil Department of General Pathology, Biological Sciences Center, State University of Londrina – UEL, Rodovia Celso Garcia Cid, Londrina, Paraná 86057-970, Brazil
Tiago Henrique Zaninelli
Affiliation:
Department of General Biology, Biological Sciences Center, State University of Londrina – UEL, Rodovia Celso Garcia Cid, Londrina, Paraná 86057-970, Brazil Department of General Pathology, Biological Sciences Center, State University of Londrina – UEL, Rodovia Celso Garcia Cid, Londrina, Paraná 86057-970, Brazil
Waldiceu Aparecido Verri
Affiliation:
Department of General Biology, Biological Sciences Center, State University of Londrina – UEL, Rodovia Celso Garcia Cid, Londrina, Paraná 86057-970, Brazil Department of General Pathology, Biological Sciences Center, State University of Londrina – UEL, Rodovia Celso Garcia Cid, Londrina, Paraná 86057-970, Brazil
Glaura Scantamburlo Alves Fernandes
Affiliation:
Department of General Biology, Biological Sciences Center, State University of Londrina – UEL, Rodovia Celso Garcia Cid, Londrina, Paraná 86057-970, Brazil Department of General Pathology, Biological Sciences Center, State University of Londrina – UEL, Rodovia Celso Garcia Cid, Londrina, Paraná 86057-970, Brazil
*
Address for correspondence: Rafaela Pires Erthal, Department of General Pathology, Biological Sciences Center, State University of Londrina – UEL, Rodovia Celso Garcia Cid, Londrina, Paraná 86057-970, Brazil. Email: rafaelaperthal@gmail.com

Abstract

Malathion is an insecticide that is used to control arboviruses and agricultural pests. Adolescents that are exposed to this insecticide are the most vulnerable as they are in the critical period of postnatal sexual development. This study aimed to evaluate whether malathion damage can affect sperm function and its respective mechanisms when adolescents are exposed during postnatal sexual development. Twenty-four male Wistar rats (PND 25) were divided into three experimental groups and treated daily for 40 d: control group (saline 0.9%), 10 mg/kg (M10 group), or 50 mg/kg (M50 group) of malathion. At PND 65, the rats were anesthetized and euthanized. Testicles were collected for the evaluation of gene expression. Sperm cells from the epididymis were used for evaluation of the oxidative profile or spermatic function. Data showed that a lower dose of malathion downregulated the gene expression of androgen receptors and testosterone converter enzyme 17-β-HSD in the testis. The acrosomal integrity of sperm cells was compromised in the M50 group, but not the M10 group. The mitochondrial activity was not impaired by exposure. Finally, although no alterations in malondialdehyde and glutathione levels were observed, malathion, at both doses, increased antioxidant enzyme catalase activity and, at a higher dose, superoxide dismutase activity. The present study showed that low doses of malathion considered to be inoffensive are capable of impairing sperm quality and function through the downregulation of testicular genic expression of AR enzyme 17-β-HSD and can damage the spermatic antioxidant profile during critical periods of development.

Type
Original Article
Copyright
© The Author(s), 2022. Published by Cambridge University Press in association with International Society for Developmental Origins of Health and Disease

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