The novel ruthenium—γ-linolenic complex [Ru2(aGLA)4Cl] inhibits C6 rat glioma cell proliferation and induces changes in mitochondrial membrane potential, increased reactive oxygen species generation and apoptosis in vitro (2010)
- Autores:
- Autores USP: COLQUHOUN, ALISON - ICB ; SILVA, DENISE DE OLIVEIRA - IQ
- Unidades: ICB; IQ
- DOI: 10.1002/cbf.1626
- Assunto: HISTOLOGIA
- Idioma: Inglês
- Imprenta:
- Local: Chichester
- Data de publicação: 2010
- Fonte:
- Título do periódico: Cell Biochemistry and Function
- ISSN: 0263-6484
- Volume/Número/Paginação/Ano: v. 28, n. 1, p. 15-23, 2010
- Este periódico é de assinatura
- Este artigo NÃO é de acesso aberto
- Cor do Acesso Aberto: closed
-
ABNT
RIBEIRO, Geise et al. The novel ruthenium—γ-linolenic complex [Ru2(aGLA)4Cl] inhibits C6 rat glioma cell proliferation and induces changes in mitochondrial membrane potential, increased reactive oxygen species generation and apoptosis in vitro. Cell Biochemistry and Function, v. 28, n. 1, p. 15-23, 2010Tradução . . Disponível em: https://doi.org/10.1002/cbf.1626. Acesso em: 16 maio 2024. -
APA
Ribeiro, G., Benadiba, M., Silva, D. de O., & Colquhoun, A. (2010). The novel ruthenium—γ-linolenic complex [Ru2(aGLA)4Cl] inhibits C6 rat glioma cell proliferation and induces changes in mitochondrial membrane potential, increased reactive oxygen species generation and apoptosis in vitro. Cell Biochemistry and Function, 28( 1), 15-23. doi:10.1002/cbf.1626 -
NLM
Ribeiro G, Benadiba M, Silva D de O, Colquhoun A. The novel ruthenium—γ-linolenic complex [Ru2(aGLA)4Cl] inhibits C6 rat glioma cell proliferation and induces changes in mitochondrial membrane potential, increased reactive oxygen species generation and apoptosis in vitro [Internet]. Cell Biochemistry and Function. 2010 ; 28( 1): 15-23.[citado 2024 maio 16 ] Available from: https://doi.org/10.1002/cbf.1626 -
Vancouver
Ribeiro G, Benadiba M, Silva D de O, Colquhoun A. The novel ruthenium—γ-linolenic complex [Ru2(aGLA)4Cl] inhibits C6 rat glioma cell proliferation and induces changes in mitochondrial membrane potential, increased reactive oxygen species generation and apoptosis in vitro [Internet]. Cell Biochemistry and Function. 2010 ; 28( 1): 15-23.[citado 2024 maio 16 ] Available from: https://doi.org/10.1002/cbf.1626 - Time-dependent effects of a novel ruthenium complex containing the non-steroidal anti-inflammatory drug (NSAID) ibuprofen on the mRNA expression of proteins involved in cell cycle control, angiogenesis and invasion in C6 rat glioma cells in vitro
- Time-dependent effects of a novel ruthenium complex containing the non-steroidal anti-inflammatory drug (nsaid) ibuprofen on the mRNA expression of proteins involved in cell cycle control, Angiogenesis and Invasion in C6 rat glioma cells in vitro
- Diruthenium(II,III)-non-steroidal anti-inflammatory drug complexes and their effects on tumor-cell proliferation
- Anti-tumour properties of novel ruthenium complexes containing non-steroidal anti-inflamatory drugs (NSAIDs)
- Inhibition of C6 rat glioma proliferation by ['RU IND. 2''CL''(ibp) IND. 4'] depends on changes in p21, p27, Bax/Bcl2 ratio and mitochondrial membrane potential
- Diruthenium(II, III) complexes of ibuprofen, aspirin, naproxen and indomethacin non-steroidal anti-inflammatory drugs: synthesis, characterization and their effects on tumor-cell proliferation
- Axially-modified paddlewheel diruthenium(II,III)-ibuprofenato metallodrugs and the influence of the structural modification on U87MG and A172 human glioma cell proliferation, apoptosis, mitosis and migration
- Synthesis and characterization of new diruthenium (II, III) complexes with non-steroidal anti-inflammatory drugs
- Diruthenium (II,III)-ketoprofen anticancer metallodrug investigated for interaction with transferrin and for effects on the antiproliferative activity, apoptotic and mitotic processes in the A172 human glioma cell line
- Growth inhibitory effects of the diruthenium-ibuprofen compound, 'RU IND. 2''CL'(Ibp)' IND. 4', in human glioma cells in vitro and in the rat C6 orthotopic glioma in vivo
Informações sobre o DOI: 10.1002/cbf.1626 (Fonte: oaDOI API)
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