'N POT.1'-acetyl-'N POT.2'-formyl-5-methoxykynuramine: a Metabolite of melatonin with strong biological activities (2004)
- Autores:
- Autores USP: MENDES, JOAO GUSTAVO PESSINI AMARANTE - ICB ; CAMPA, ANA - FCF
- Unidades: ICB; FCF
- Assunto: IMUNOLOGIA
- Idioma: Inglês
- Resumo: Inammation triggers the synthesis of a great number of immunomodulatory compounds. We have hypothesized that melatonin and derivatives are some of these compounds. This hypothesis is mainly supported by the e_cient synthesis and further oxidation of melatonin by activated-immune cells in vitro and the antiinammatory activity of melatonin in vivo. In order to verify if inammation leads to melatonin oxidation in vivo, we analyzed the cerebrospinal uid (CSF) of patients with meningitis. High-performance liquid chromatograph with uorescence detection was used to detect the melatonin oxidation product N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK) in dicholomethane extracted- CSF. AFMK was found in 10 from 13 CSF samples of patients with viral meningitis and in none of 8 control samples. In sequence we evaluated if the release of the proinammatory cytokines interleukin- 8 (IL-8) and tumor necrosis factor-_ (TNF-_) by neutrophils and cell apoptosis were modi_ed by melatonin, AFMK and AMK (derived from AFMK demethylation). The concentration of cytokines released in the supernatant of cultured lipopolysaccharide (LPS)-activated human blood neutrophils was determined by ELISA and apoptosis by ow cytometry (annexin V/PI). All the compounds assayed (at the concentration range of 0.001 to 1 mM) e_ciently inhibit the production of IL-8 and TNF-_ by LPS-activated neutrophils. AFMK caused the most e_ective inhibition. A signi_cant inhibition of neutrophil apoptosis (approximately30 %) was triggered by AFMK and AMK (1 mM) but not by melatonin. We concluded that AFMK is formed in vivo in inammatory conditions and that neutrophils are an important target for AFMK. The formation of AFMK may play a role in the beginning of the inammatory process through the control of neutrophils life span and activity and,the refore, in the conduction of the disease
- Imprenta:
- Fonte:
- Título do periódico: Programa e resumos
- Nome do evento: Sociedade Brasileira de Bioquímica e Biologia Molecular - SBBq
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ABNT
SILVA, Sueli de Oliveira et al. 'N POT.1'-acetyl-'N POT.2'-formyl-5-methoxykynuramine: a Metabolite of melatonin with strong biological activities. 2004, Anais.. Caxambu: Instituto de Ciências Biomédicas, Universidade de São Paulo, 2004. . Acesso em: 19 abr. 2024. -
APA
Silva, S. de O., Ximenes, V. F., Bueno-da-Silva, A. E. B., Amarante-Mendes, J. G. P., & Campa, A. (2004). 'N POT.1'-acetyl-'N POT.2'-formyl-5-methoxykynuramine: a Metabolite of melatonin with strong biological activities. In Programa e resumos. Caxambu: Instituto de Ciências Biomédicas, Universidade de São Paulo. -
NLM
Silva S de O, Ximenes VF, Bueno-da-Silva AEB, Amarante-Mendes JGP, Campa A. 'N POT.1'-acetyl-'N POT.2'-formyl-5-methoxykynuramine: a Metabolite of melatonin with strong biological activities. Programa e resumos. 2004 ;[citado 2024 abr. 19 ] -
Vancouver
Silva S de O, Ximenes VF, Bueno-da-Silva AEB, Amarante-Mendes JGP, Campa A. 'N POT.1'-acetyl-'N POT.2'-formyl-5-methoxykynuramine: a Metabolite of melatonin with strong biological activities. Programa e resumos. 2004 ;[citado 2024 abr. 19 ] - 'N POT.1'-acetyl-'N POT.2'-formyl-5-methoxykynuramine: a metabolite of melatonin with strong biological activities
- Melatonin inhibits fas ligand expression and protects T cells from activation-induced cell death: role of NFAT signaling pathway
- Immune modulatory actions of tryptophan and melatonin metabolites
- A new view for the antiinflammatory effect of melatonin
- Melatonin and its oxidation product inhibit fasl expression and protects T cells from activation-induced celldeath
- Neutrophils as a specific target for melatonin and kynuramines: effects on cytokine release
- Melatonin and its oxidation product AFMK inhibit FasL expression and protects T cells from activation-induced cell death
- Melatonin protects CD4+ T cells from activation induced cell death by blocking nfat mediated CD95l uppregulation
- Melatonin protects CD4+ T cells from activation-induced cell death by blocking NFAT-mediated CD95 ligand upregulation
- Melatonin and its oxidation product inhibit FasL expression and protects T cells from activation-induced cell death
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