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Glutathione regulation of tumor necrosis factor-alpha-induced NF-kappa B activation in skeletal muscle-derived L6 cells.
Biochem Biophys Res Commun. 1997 Aug 28; 237(3):645-9.BB

Abstract

TNF alpha is implicated in several skeletal muscle pathologies including muscle wasting of cachexia. Muscle wasting and other conditions such as physical exercise and immobilization are also associated with disturbances in muscle glutathione status. Hence, it was of interest to investigate the role of endogenous glutathione status in TNF alpha induced NF-kappa B activation in skeletal muscle-derived cells. TNF alpha proved to be a potent inducer of transient NF-kappa B activation in L6 myoblasts. In buthioninesulfoximine (BSO) treated cells, TNF alpha induced NF-kappa B activation was markedly potentiated suggesting that such activation is sensitive to cellular GSH, but may have been independent of high levels of intracellular GSSG. Because this activation was inhibited by the antioxidant pyrrolidinedithiocarbamate (PDTC) the involvement of reactive oxygen species in this activation system seems likely. NF-kappa B activation in L6 cells was also observed in response to direct H2O2 treatment. Results from GSSG reductase inhibited cells suggest that GSSG may participate in, but is not required for, TNF alpha induced NF-kappa B activation. The inhibitory effect of PDTC on NF-kappa B activation correlated with its effect on ICAM-1 expression suggesting that this GSH status modifying agent not only influenced nuclear translocation of NF-kappa B proteins but also regulated kappa B dependent transcription.

Authors+Show Affiliations

Department of Molecular and Cell Biology, University of California at Berkeley 94720, USA. cksen@socrates.berkeley.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

9299419

Citation

Sen, C K., et al. "Glutathione Regulation of Tumor Necrosis Factor-alpha-induced NF-kappa B Activation in Skeletal Muscle-derived L6 Cells." Biochemical and Biophysical Research Communications, vol. 237, no. 3, 1997, pp. 645-9.
Sen CK, Khanna S, Reznick AZ, et al. Glutathione regulation of tumor necrosis factor-alpha-induced NF-kappa B activation in skeletal muscle-derived L6 cells. Biochem Biophys Res Commun. 1997;237(3):645-9.
Sen, C. K., Khanna, S., Reznick, A. Z., Roy, S., & Packer, L. (1997). Glutathione regulation of tumor necrosis factor-alpha-induced NF-kappa B activation in skeletal muscle-derived L6 cells. Biochemical and Biophysical Research Communications, 237(3), 645-9.
Sen CK, et al. Glutathione Regulation of Tumor Necrosis Factor-alpha-induced NF-kappa B Activation in Skeletal Muscle-derived L6 Cells. Biochem Biophys Res Commun. 1997 Aug 28;237(3):645-9. PubMed PMID: 9299419.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glutathione regulation of tumor necrosis factor-alpha-induced NF-kappa B activation in skeletal muscle-derived L6 cells. AU - Sen,C K, AU - Khanna,S, AU - Reznick,A Z, AU - Roy,S, AU - Packer,L, PY - 1997/8/28/pubmed PY - 1997/9/23/medline PY - 1997/8/28/entrez SP - 645 EP - 9 JF - Biochemical and biophysical research communications JO - Biochem Biophys Res Commun VL - 237 IS - 3 N2 - TNF alpha is implicated in several skeletal muscle pathologies including muscle wasting of cachexia. Muscle wasting and other conditions such as physical exercise and immobilization are also associated with disturbances in muscle glutathione status. Hence, it was of interest to investigate the role of endogenous glutathione status in TNF alpha induced NF-kappa B activation in skeletal muscle-derived cells. TNF alpha proved to be a potent inducer of transient NF-kappa B activation in L6 myoblasts. In buthioninesulfoximine (BSO) treated cells, TNF alpha induced NF-kappa B activation was markedly potentiated suggesting that such activation is sensitive to cellular GSH, but may have been independent of high levels of intracellular GSSG. Because this activation was inhibited by the antioxidant pyrrolidinedithiocarbamate (PDTC) the involvement of reactive oxygen species in this activation system seems likely. NF-kappa B activation in L6 cells was also observed in response to direct H2O2 treatment. Results from GSSG reductase inhibited cells suggest that GSSG may participate in, but is not required for, TNF alpha induced NF-kappa B activation. The inhibitory effect of PDTC on NF-kappa B activation correlated with its effect on ICAM-1 expression suggesting that this GSH status modifying agent not only influenced nuclear translocation of NF-kappa B proteins but also regulated kappa B dependent transcription. SN - 0006-291X UR - https://www.unboundmedicine.com/medline/citation/9299419/Glutathione_regulation_of_tumor_necrosis_factor_alpha_induced_NF_kappa_B_activation_in_skeletal_muscle_derived_L6_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-291X(97)97206-5 DB - PRIME DP - Unbound Medicine ER -