Efeitos da exposição pré e pós-natal de MALATHION sobre o neurodesenvolvimento: possível associação causal com o comportamento autista

• Ano de defesa: 2017
• Autor(a) principal: Souza, Diego Anacleto de
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Palavras-chave em Português: Neurodesenvolvimento; Organofosforado; TEA
• Link de acesso: https://repositorio.animaeducacao.com.br/handle/ANIMA/3056

Exposure to organophosphorus pesticides (OPs), including malathion, is associated with the pathophysiology of neurological diseases, such as Autistic Spectrum Disorder (ASD). ASD is a neuropsychiatric disorder manifested by qualitative impairments in reciprocal social interaction, associated with motor disorders such as stereotypies and restricted interest. Due to the increased prevalence of ASD based on studies suggesting the contribution of OP to the pathophysiology of this disorder, it was aimed to evaluate the ontogenetic and behavioral effects of pre and postnatal exposure to malathion in Wistar rats. Pregnant females were divided into two groups: prenatal, received malathion (200mg / kg) per gavage on gestational days (DG) 06-14 and those receiving malathion during the lactation period (21 days). The control groups received vehicle in the period and volume equivalent. During the first 21 postnatal days, the offspring prenatally exposed to malathion were submitted to the analysis of ontogenetic and reflexological parameters. Sexing occurred shortly after the analysis of reflex ontogenesis. In postnatal day (PND) 30, 45 and 60, males exposed in both the pre- and postnatal periods were submitted to behavioral and cognitive parameters analyzes. The results showed that prenatal exposure to malathion caused significant behavioral changes characterized by hyperactivity, increased stereotyped movements and social impairment, as well as cognitive impairment related to animal memory. There were no changes in the physical development of the offspring exposed to malathion in relation to the control group, suggesting that the damage caused by the early exposure to malathion is exclusively neurological. The behavioral parameters affected by prenatal exposure to malathion also became impaired after postnatal exposure. The changes observed in this study are compatible with the symptomatology of patients with ASD. The understanding of these effects alerts to the use of this compound due to its neurotoxic potential and reinforces the environmental contribution of OP in the pathophysiology of neurological diseases, such as ASD.