Evidence map›Paper›PMID 39826055›Full record

ArticleMetabolic brain disease2025

L-carnitine protects against oxidative damage and neuroinflammation in cerebral cortex of rats submitted to chronic chemically-induced model of hyperphenylalaninemia.

Jéssica Lamberty Faverzani, Gilian Guerreiro, Franciele Fatima Lopes, Angela Sitta, Daniella de Moura Coelho, Caroline Paula Mescka, Luísa Degrandi Sehn, Gabriel de Lima Rosa, Amanda Muliterno Domingues Lourenço de Lima, Esteban Alberto Gonzalez and 6 more

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Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Jéssica Lamberty FaverzaniPrograma de Pós-Graduação em Ciências Farmacêuticas, Universidade Federal do Rio Grande do Sul, Avenida Ipiranga, 2752, Porto Alegre, CEP 90610-000, RS, Brazil. jelamberty@hotmail.com.
Gilian GuerreiroServiço de Genética Médica, Hospital de Clínicas de Porto Alegre, Rua Ramiro Barcelos, Porto Alegre, 2350, CEP 90035-003, RS, Brazil.
Franciele Fatima LopesPrograma de Pós-Graduação em Ciências Farmacêuticas, Universidade Federal do Rio Grande do Sul, Avenida Ipiranga, 2752, Porto Alegre, CEP 90610-000, RS, Brazil.
Angela SittaServiço de Genética Médica, Hospital de Clínicas de Porto Alegre, Rua Ramiro Barcelos, Porto Alegre, 2350, CEP 90035-003, RS, Brazil.
Daniella de Moura CoelhoServiço de Genética Médica, Hospital de Clínicas de Porto Alegre, Rua Ramiro Barcelos, Porto Alegre, 2350, CEP 90035-003, RS, Brazil.
Caroline Paula MesckaServiço de Genética Médica, Hospital de Clínicas de Porto Alegre, Rua Ramiro Barcelos, Porto Alegre, 2350, CEP 90035-003, RS, Brazil.
Luísa Degrandi SehnServiço de Genética Médica, Hospital de Clínicas de Porto Alegre, Rua Ramiro Barcelos, Porto Alegre, 2350, CEP 90035-003, RS, Brazil.
Gabriel de Lima RosaPrograma de Pós-Graduação em Ciências Biológicas, Fisiologia, Instituto de Ciências Básicas e da Saúde, Universidade Federal do Rio Grande do Sul, Rua Sarmento Leite, 500, Porto Alegre, CEP 90050- 170, RS, Brazil.
Amanda Muliterno Domingues Lourenço de LimaPrograma de Pós-Graduação em Ciências Biológicas, Fisiologia, Instituto de Ciências Básicas e da Saúde, Universidade Federal do Rio Grande do Sul, Rua Sarmento Leite, 500, Porto Alegre, CEP 90050- 170, RS, Brazil.
Esteban Alberto GonzalezLaboratório de Células, Tecidos e Genes, Centro de Pesquisa Experimental, Hospital de Clínicas de Porto Alegre, Rua Ramiro Barcelos, 2350, Porto Alegre, CEP 90035-003, RS, Brazil.
Rafael Teixeira RibeiroPrograma de Pós-Graduação em Ciências Biológicas: Bioquímica, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos, 2600, Porto Alegre, CEP 90035-003, RS, Brazil.
Rafael PalavroPrograma de Pós-Graduação em Ciências Biológicas: Bioquímica, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos, 2600, Porto Alegre, CEP 90035-003, RS, Brazil.
Adriana Simon CoitinhoPrograma de Pós-Graduação em Ciências Biológicas, Fisiologia, Instituto de Ciências Básicas e da Saúde, Universidade Federal do Rio Grande do Sul, Rua Sarmento Leite, 500, Porto Alegre, CEP 90050- 170, RS, Brazil.
Guilherme BaldoPrograma de Pós-Graduação em Ciências Biológicas, Fisiologia, Instituto de Ciências Básicas e da Saúde, Universidade Federal do Rio Grande do Sul, Rua Sarmento Leite, 500, Porto Alegre, CEP 90050- 170, RS, Brazil.
Moacir WajnerServiço de Genética Médica, Hospital de Clínicas de Porto Alegre, Rua Ramiro Barcelos, Porto Alegre, 2350, CEP 90035-003, RS, Brazil.
Carmen Regla VargasPrograma de Pós-Graduação em Ciências Farmacêuticas, Universidade Federal do Rio Grande do Sul, Avenida Ipiranga, 2752, Porto Alegre, CEP 90610-000, RS, Brazil. crvargas@hcpa.edu.br.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phenylketonuria is a genetic disorder characterized by high phenylalanine levels, the main toxic metabolite of the disease. Hyperphenylalaninemia can cause neurological impairment. In order to avoid this symptomatology, patients typically follow a phenylalanine-free diet supplemented with a synthetic formula that provides essential amino acids, including L-carnitine. This work aims to evaluate the potential neuroprotective effects of L-carnitine treatment in the cerebral cortex of rats submitted to a chronic chemically-induced model of Hyperphenylalaninemia, evaluating brain oxidative damage and neuroinflammation. We confirm the effectiveness of the animal model, through the increase of phenylalanine and L-carnitine in blood and cerebral cortex. L-carnitine treatment was effective in significantly decreasing the generation of reactive species and attenuating the superoxide dismutase (SOD) activity. Significant negative correlations between L-carnitine and superoxide dismutase as well as L-carnitine and reactive species generation were also found, reinforcing the involvement of oxidative stress and the effect of L-carnitine. Besides, L-carnitine attenuated the decrease in IL-4 levels, demonstrating both anti-inflammatory properties and a neuroprotective effect, through the decrease in the overexpression of the glial fibrillary acidic protein (GFAP) present in the cerebral cortex of rats with Hyperphenylalaninemia. Our results highlight the neuroprotective role of L-carnitine in the treatment of Phenylketonuria, mainly against neuroinflammation and the oxidative process, contributing to better clarify the pathophysiology of the disease.

Indexed as

CarnitineCerebral CortexNeuroinflammatory DiseasesNeuroprotective AgentsOxidative StressPhenylketonuriasAnimalsDisease Models, AnimalMalePhenylalanineRatsRats, WistarSuperoxide DismutaseCarnitineNeuroprotective AgentsPhenylalanineSuperoxide DismutaseGlial fibrillary acidic proteinHyperphenylalaninemiaL-carnitineNeuroinflammationOxidative stressPhenylketonuria

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.