ArticleMetabolic brain disease2015
The characterization of neuroenergetic effects of chronic L-tyrosine administration in young rats: evidence for striatal susceptibility.
Article in Metabolic brain disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- Experimental evidence of tyrosine neurotoxicity: focus on mitochondrial dysfunction.Metabolic brain disease · 2021Review
- Towards resolving the enigma of the dichotomy of resveratrol: cis- and trans-resveratrol have opposite effects on TyrRS-regulated PARP1 activation.GeroScience · 2021Article
- Effects of omega-3 fatty acids supplementation on inflammatory parameters after chronic administration of L-tyrosine.Metabolic brain disease · 2020Article
- Evidence of hippocampal astrogliosis and antioxidant imbalance after L-tyrosine chronic administration in rats.Metabolic brain disease · 2020Article
- Omega-3 fatty acid supplementation can prevent changes in mitochondrial energy metabolism and oxidative stress caused by chronic administration of L-tyrosine in the brain of rats.Metabolic brain disease · 2019Article
- Antioxidants Reverse the Changes in the Cholinergic System Caused by L-Tyrosine Administration in Rats.Neurotoxicity research · 2018Article
- Role of antioxidant treatment on DNA and lipid damage in the brain of rats subjected to a chemically induced chronic model of tyrosinemia type II.Molecular and cellular biochemistry · 2017Article
- Omega-3 fatty acid supplementation decreases DNA damage in brain of rats subjected to a chemically induced chronic model of Tyrosinemia type II.Metabolic brain disease · 2017Article
- Long-term cognitive functioning in individuals with tyrosinemia type 1 treated with nitisinone and protein-restricted diet.Molecular genetics and metabolism reports · 2017Article
- Antioxidants reverse the changes in energy metabolism of rat brain after chronic administration of L.-tyrosine.Metabolic brain disease · 2017Article
- A Novel Genetic Screen Identifies Modifiers of Age-Dependent Amyloid β Toxicity in theFrontiers in aging neuroscience · 2017Article
- In Vivo NMR Studies of the Brain with Hereditary or Acquired Metabolic Disorders.Neurochemical research · 2015Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tyrosinemia type II is an inborn error of metabolism caused by a deficiency in hepatic cytosolic aminotransferase. Affected patients usually present a variable degree of mental retardation, which may be related to the level of plasma tyrosine. In the present study we evaluated effect of chronic administration of L-tyrosine on the activities of citrate synthase, malate dehydrogenase, succinate dehydrogenase and complexes I, II, II-III and IV in cerebral cortex, hippocampus and striatum of rats in development. Chronic administration consisted of L-tyrosine (500 mg/kg) or saline injections 12 h apart for 24 days in Wistar rats (7 days old); rats were killed 12 h after last injection. Our results demonstrated that L-tyrosine inhibited the activity of citrate synthase in the hippocampus and striatum, malate dehydrogenase activity was increased in striatum and succinate dehydrogenase, complexes I and II-III activities were inhibited in striatum. However, complex IV activity was increased in hippocampus and inhibited in striatum. By these findings, we suggest that repeated administrations of L-tyrosine cause alterations in energy metabolism, which may be similar to the acute administration in brain of infant rats. Taking together the present findings and evidence from the literature, we hypothesize that energy metabolism impairment could be considered an important pathophysiological mechanism underlying the brain damage observed in patients with tyrosinemia type II.
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