作者: Rafaela Antonini , Giselli Scaini , Monique Michels , Mariane BD Matias , Patrícia F Schuck
DOI: 10.1007/S11011-019-00525-X
关键词:
摘要: Tyrosinemia type II is an autosomal recessive inborn error of metabolism caused by hepatic cytosolic tyrosine aminotransferase deficiency. Importantly, this disease associated with neurological and developmental abnormalities in many patients. Considering that the mechanisms underlying dysfunction hypertyrosinemic patients are poorly understood, present work we investigated levels cytokines - tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 IL-10 cerebellum, hippocampus, striatum young rats exposed to chronic administration L-tyrosine. In addition, also impact supplementation Omega-3 fatty acids (n-3 PUFA) on rodent model Tyrosinemia. Notably, previous study demonstrated association between L-tyrosine toxicity n-3 PUFA Our results showed a significant increase pro- anti-inflammatory brain structures when animals were administered Cerebral cortex seem be more susceptible inflammation induced toxicity. attenuated alterations exposure regions infant rats. conclusion, important process related neurotoxicity observed experimental Finally, could considered as potential neuroprotective adjunctive therapy for Tyrosinemias, especially II.