ArticleNeurochemical research2014
L-tyrosine induces DNA damage in brain and blood of rats.
Article in Neurochemical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Behavioral Alterations and Cholinergic Modulation in Zebrafish Acutely Exposed To Tyrosine.Neurotoxicity research · 2025Article
- Nitisinone treatment protect hereditary tyrosinemia type I patients against inflammation, DNA and protein oxidative damage by decreasing succinylacetone levels.Metabolic brain disease · 2025Article
- Exploring the Prevention of Lipid Deposition Caused by High-Fat Diet and Its Mechanism of Action ofFood science & nutrition · 2025Article
- Evaluation of dynamic thiol/disulfide homeostasis in hereditary tyrosinemia type 1 patients.Pediatric research · 2022Article
- Cis- and trans-resveratrol have opposite effects on histone serine-ADP-ribosylation and tyrosine induced neurodegeneration.Nature communications · 2022Article
- Toxicity ofPlants (Basel, Switzerland) · 2021Review
- 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
- TYROSINEMIA TYPE III: A CASE REPORT OF SIBLINGS AND LITERATURE REVIEW.Revista paulista de pediatria : orgao oficial da Sociedade de Pediatria de Sao Paulo · 2020Review
- Blood and Brain Biochemistry and Behaviour in NTBC and Dietary Treated Tyrosinemia Type 1 Mice.Nutrients · 2019Article
- 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
- Tyrosine aminotransferase is involved in the oxidative stress response by metabolizingThe Journal of biological chemistry · 2019Article
- Antioxidants Reverse the Changes in the Cholinergic System Caused by L-Tyrosine Administration in Rats.Neurotoxicity research · 2018Article
- Serum Amino Acid Profiling in Patients with Alkaptonuria Before and After Treatment with Nitisinone.JIMD reports · 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
- Antioxidants reverse the changes in energy metabolism of rat brain after chronic administration of L.-tyrosine.Metabolic brain disease · 2017Article
- Evidence that 3-hydroxy-3-methylglutaric and 3-methylglutaric acids induce DNA damage in rat striatum.Metabolic brain disease · 2015Article
- The characterization of neuroenergetic effects of chronic L-tyrosine administration in young rats: evidence for striatal susceptibility.Metabolic brain disease · 2015Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the tyrosine aminotransferase gene have been identified to cause tyrosinemia type II which is inherited in an autosomal recessive manner. Studies have demonstrated that an excessive production of ROS can lead to reactions with macromolecules, such as DNA, lipids, and proteins. Considering that the L-tyrosine may promote oxidative stress, the main objective of this study was to investigate the in vivo effects of L-tyrosine on DNA damage determined by the alkaline comet assay, in brain and blood of rats. In our acute protocol, Wistar rats (30 days old) were killed 1 h after a single intraperitoneal L-tyrosine injection (500 mg/kg) or saline. For chronic administration, the animals received two subcutaneous injections of L-tyrosine (500 mg/kg, 12-h intervals) or saline administered for 24 days starting at postnatal day (PD) 7 (last injection at PD 31), 12 h after the last injection, the animals were killed by decapitation. We observed that acute administration of L-tyrosine increased DNA damage frequency and damage index in cerebral cortex and blood when compared to control group. Moreover, we observed that chronic administration of L-tyrosine increased DNA damage frequency and damage index in hippocampus, striatum, cerebral cortex and blood when compared to control group. In conclusion, the present work demonstrated that DNA damage can be encountered in brain from animal models of hypertyrosinemia, DNA alterations may represent a further means to explain neurological dysfunction in this inherited metabolic disorder and to reinforce the role of oxidative stress in the pathophysiology of tyrosinemia type II.
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