Administration of histidine to female rats induces changes in oxidative status in cortex and hippocampus of the offspring.

Abstract:

:Histidinemia is an inherited metabolic disorder biochemically characterized by high concentrations of histidine in biological fluids. Usually affected patients are asymptomatic although some individuals have mental retardation and speech disorders. Considering the high prevalence of histidinemia and the scarce information on the effects of maternal histidinemia on their progeny, we investigated various parameters of oxidative stress in brain cortex and hippocampus of the offspring from female rats that received histidine (0.5 mg/g of body weight) in the course of pregnancy and lactation. At 21 days of age we found a significant increase of thiobarbituric acid reactive substances (TBARS), 2',7'-dihydrodichlorofluorescein oxidation, superoxide dismutase (SOD) activity, catalase (CAT) activity, total sulfhydryls and glutathione (GSH) content in cerebral cortex and hippocampus. We also verified that at 60 days of age, GSH, SOD and total sulfhydryls returned to normal levels in brain cortex, while the other parameters decreased in the same structure. In the hippocampus, at 60 days of age GSH returned to normal levels, CAT persisted elevated and the other parameters decreased. These results indicate that histidine administration to female rats can induce oxidative stress in the brain from the offspring, which partially recovers 40 days after breastfeeding stopped.

journal_name

Neurochem Res

journal_title

Neurochemical research

authors

Rojas DB,Gemelli T,de Andrade RB,Campos AG,Dutra-Filho CS,Wannmacher CM

doi

10.1007/s11064-012-0703-7

subject

Has Abstract

pub_date

2012-05-01 00:00:00

pages

1031-6

issue

5

eissn

0364-3190

issn

1573-6903

journal_volume

37

pub_type

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