Effect of histidine administration to female rats during pregnancy and lactation on enzymes activity of phosphoryltransfer network in cerebral cortex and hippocampus of the offspring

• Published in: Metabolic brain disease Vol. 27; no. 4; pp. 595 - 603
• Main Authors: Rojas, Denise Bertin, de Andrade, Rodrigo Binkowski, Gemelli, Tanise, Oliveira, Lenise Santos, Campos, Aline Guimarães, Dutra-Filho, Carlos Severo, Wannmacher, Clóvis Milton Duval
• Format: Journal Article
• Language: English
• Published: Boston Springer US 01.12.2012; Springer Nature B.V
• Subjects: Adenylate kinase; Adenylate Kinase - metabolism; Age; Amino acids; Animals; Biochemistry; Biomedical and Life Sciences; Biomedicine; Cerebral Cortex - drug effects; Cerebral Cortex - metabolism; Children; Cortex; Creatine kinase; Creatine Kinase - metabolism; Energy balance; Energy Metabolism - drug effects; Enzymes; Female; Hippocampus; Hippocampus - drug effects; Hippocampus - metabolism; Histidine; Histidine - blood; Histidine - pharmacology; Histidinemia; Inborn errors of metabolism; Lactation; Lactation - drug effects; Liver; Male; Metabolic Diseases; Metabolic disorders; Mitochondria; Nerve Tissue Proteins - analysis; Nerve Tissue Proteins - biosynthesis; Neurology; Neurosciences; Oncology; Original Paper; Pregnancy; Pregnancy, Animal - drug effects; Progeny; Pyruvate kinase; Pyruvate Kinase - metabolism; Rats; Rats, Wistar; L-histidine; Energy metabolism; Pyruvate kinase; Adenylate kinase; Creatine kinase; Maternal histidinemia
• ISSN: 0885-7490; 1573-7365
• DOI: 10.1007/s11011-012-9319-5

Histidinemia is an inborn error of metabolism of amino acids caused by deficiency of histidase activity in liver and skin with consequent accumulation of histidine in plasma and tissues. Histidinemia is an autosomal recessive trait usually considered harmless to patients and their offspring, but some patients and children born from histidinemic mothers have mild neurologic alterations. Considering that histidinemia is one of the most frequently identified metabolic conditions, in the present study we investigated the effect of L-histidine load to female rats during pregnancy and lactation on some parameters of phosphoryltransfer network in cerebral cortex and hippocampus of the offspring. Pyruvate kinase, cytosolic and mitochondrial creatine kinase activities decreased in cerebral cortex and in hippocampus of rats at 21 days of age and this pattern remained in the cerebral cortex and in hippocampus at 60 days of age. Moreover, adenylate kinase activity was reduced in the cerebral cortex and in hippocampus of the offspring at 21 days of age, whereas the activity was increased in the two tissues at 60 days of age. These results suggest that administration of L-histidine to female rats in the course of pregnancy and lactation could impair energy homeostasis in the cerebral cortex and hippocampus of the offspring. Considering that histidinemia is usually a benign condition and little attention has been given to maternal histidinemia, it seems important to perform more studies in the children born from histidinemic mothers.