Journal ArticleDOI
Biologic and pharmacologic regulation of mammalian glutathione synthesis.
TLDR
Because GSH plays a critical role in cellular defenses against electrophiles, oxidative stress and nitrosating species, pharmacologic manipulation of GSH synthesis has received much attention.About:
This article is published in Free Radical Biology and Medicine.The article was published on 1999-11-01. It has received 1120 citations till now. The article focuses on the topics: Glutathione & Buthionine sulfoximine.read more
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Journal ArticleDOI
N-acetylcysteine ethyl ester as GSH enhancer in human primary endothelial cells: A comparative study with other drugs.
Daniela Giustarini,Federico Galvagni,Isabella Dalle Donne,Aldo Milzani,Filiberto Maria Severi,Annalisa Santucci,Ranieri Rossi +6 more
TL;DR: It is demonstrated that the slight increase in intracellular levels of cysteine and GSH induced by NAC in HUVEC grown in standard medium was due to the reduction of the cystine present in the medium itself there rather than to the action of NAC as Cys pro‐drug.
Journal ArticleDOI
Induction of glutathione synthesis explains pharmacodynamics of high-dose busulfan in mice and highlights putative mechanisms of drug interaction
Jérôme Bouligand,Alain Deroussent,Nicolas Simonnard,Paule Opolon,Jackie Morizet,Elisabeth Connault,Estelle Daudigeos,Micheline Re,Angelo Paci,Gilles Vassal +9 more
TL;DR: This is the first time that in vivo flux of GSH synthesis has been shown to be closely related to a drug plasma clearance and toxicity in mice, and allows hypothesizing that GSH liver synthesis may directly influence busulfan clearance in humans.
Journal ArticleDOI
Cell-density-dependent methylmercury susceptibility of cultured human brain microvascular pericytes
Takashi Hirooka,Yasuyuki Fujiwara,Yuka Minami,Akihiko Ishii,Mio Ishigooka,Yasuhiro Shinkai,Chika Yamamoto,Masahiko Satoh,Akira Yasutake,Komyo Eto,Toshiyuki Kaji +10 more
TL;DR: The present data revealed that pericytes are markedly susceptible to methylmercury-induced cytotoxicity at low cell densities, and this susceptibility is postulated to be due to the not only constitutively higher but also methyl MERCury- induced expression of LAT 1, which increased the intracellular accumulation of methylmerCury.
Journal ArticleDOI
Relating diving behavior and antioxidant status: Insights from oxidative stress biomarkers in the blood of two distinct divers, Mirounga leonina and Arctocephalus australis.
TL;DR: The constitutive antioxidant defenses of both species are of distinct magnitudes due to their inherent diving capacity, suggesting that higher antioxidant content is needed to counteract the high ROS production associated with the long submergence times of these mammals.
Journal ArticleDOI
UVB light suppresses nitric oxide production by murine keratinocytes and macrophages.
TL;DR: UVB light functions to suppress NOS2 gene expression in macrophages by inhibiting the activity of key regulatory transcription factors, in contrast, in keratinocytes, inhibition occurs downstream of Nos2 promoter activity.
References
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The metabolic basis of inherited disease
TL;DR: The metabolic basis of inherited disease, the metabolic basis for inherited disease as mentioned in this paper, The metabolic basis in inherited disease and inherited diseases, and inherited disease diagnosis and management, in the context of inherited diseases
Journal ArticleDOI
Antioxidant and Redox Regulation of Gene Transcription
Chandan K. Sen,Lester Packer +1 more
TL;DR: The efficacy of different antioxidants to favorably influence the molecular mechanisms implicated in human disease should be a critical determinant of its selection for clinical studies.
Journal ArticleDOI
Efficacy of oral N-acetylcysteine in the treatment of acetaminophen overdose. Analysis of the national multicenter study (1976 to 1985)
TL;DR: It is concluded that N-acetylcysteine treatment should be started within eight hours of an acetaminophen overdose, but that treatment is still indicated at least as late as 24 hours after ingestion, and it may be superior when treatment is delayed.