Glutathione deficiency and HIV

Buhl, Roland; Jaffe, Howard; Holroyd, K J; Wells, FaithB.; Mastrangeli, Andrea; Saltini, Cesare; Cantin, AndreM.; Crystal, R. G.

doi:10.1016/0140-6736(90)90783-2

Cited by 18 publications

(13 citation statements)

References 2 publications

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“…Buhl et al [3] confirmed these results, further demonstrating that the lung epithelial lining fluid from HIV-infected individuals had se verely depleted glutathione levels.…”

Section: Introductionsupporting

confidence: 76%

“…The decreased glutathione levels shown by Eck et al [2] and Buhl et al [3] were measured in serum samples or bulk lysates of cells. We adapted a fluorescence-activated cell sorter (FACS)-based assay [52] to measure intracel lular glutathione on a cell-by-cell basis in PBMC, in order to study the depletion in greater depth.…”

Section: Hiv-infected Individuals Have Depleted Glutathione Levelsmentioning

confidence: 99%

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N-Acetylcysteine: Potential for AIDS Therapy

Ela¹,

Herzenberg²

1993

Pharmacology

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The observations that people infected with HIV suffer not only from an inflammatory stress but also from depleted glutathione levels have led to a general hypothesis that these two are causally related, and that treatment of AIDS should include thiol-replenishment therapy. In particular, inflammatory stimulations are dependent on intracellular thiol levels, as they are potentiated at low glutathione levels (oxidative stress) and inhibited at high glutathione levels. Inflammatory stress may itself lead to decreased levels of glutathione. HIV has taken advantage of inflammatory signals to regulate its own replication; thus, the HIV infection is exacerbated by low levels of glutathione. We have shown that N-acetylcysteine can inhibit inflammatory stimulations, including that of HIV replication. Since N-acetylcysteine can replenish depleted glutathione levels in vivo, we suggest that it be used as an adjunct in the treatment of AIDS.

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“…Buhl et al [3] confirmed these results, further demonstrating that the lung epithelial lining fluid from HIV-infected individuals had se verely depleted glutathione levels.…”

Section: Introductionsupporting

confidence: 76%

Section: Hiv-infected Individuals Have Depleted Glutathione Levelsmentioning

confidence: 99%

N-Acetylcysteine: Potential for AIDS Therapy

Ela¹,

Herzenberg²

1993

Pharmacology

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“…monocytes and T-lymphocytes) (37). In addition, expression of IP-10 has been detected in alveolar macrophages (38,39). Despite the similar tissue and target cell specificity of rat CXCR1-like and IP-10, we were unable to detect rat CXCR1-like transfected cell responsiveness to application of IP-10.…”

Section: Discussioncontrasting

confidence: 37%

Identification of Two Rat Genes Orthologous to the Human Interleukin-8 Receptors

Dunstan

Salafranca

Adhikari

et al. 1996

Journal of Biological Chemistry

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The genes encoding two functional human interleukin-8 (IL-8) receptors have been identified by molecular cloning techniques and they are members of the rhodopsin G-protein coupled receptor (GCR) superfamily. We report the molecular cloning of two rat GCR genes (rat CXCR1-like and rat CXCR2) whose conceptualized amino acid sequences are approximately 70% identical to the human IL-8 A and B receptor subtypes. The murine GRO-like peptide, macrophage inflammatory peptide-2 (MIP-2), elevates intracellular calcium levels in HEK293 cells expressing the rat CXCR2 receptor. Southern blot analysis of restriction-digested rodent and human genomic DNAs indicate that rat CXCR1-like and CXCR2 are: 1) each single copy genes in the rat genome; 2) most closely related to the human IL-8 receptor genes; and 3) orthologous to two previously identified murine genes. CXCR2 mRNA is detected in adult rat lung, spleen, and neutrophils. CXCR1-like mRNA can be detected in adult rat lung, native rat macrophages, and a rat alveolar macrophage cell line (NR8383). These data identify the rat orthologs of the human IL-8 receptors, and describe cellular and tissue targets of rat C-X-C chemokine peptides.

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“…HIV-infected individuals exhibit systemic Glutathione deficiencies [36][37][38] and redox balance alterations in their CD4+ lymphocytes [39,40]. Although oxidative stress is a relevant step in many models of apoptosis [20], its role in CD95-mediated apoptosis is still debated.…”

Section: Time (H)mentioning

confidence: 99%

Apoptosis induced by HIV‐gp120 in a Th1 clone involves the generation of reactive oxygen intermediates downstream CD95 triggering

et al. 1997

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HIV-gpl20 sensitizes Thl clones from seronegative donors to apoptosis, which occurs through two distinct events: expression of CD95L followed by its interaction with CD95 to trigger cell death. gpl20-apoptosis of the Thl clone 103 was inhibited by Cyclosporin A, the PTK inhibitors Genistein and PNU152518, as well as the anti-oxidants Ascorbic Acid and Glutathione. Cyclosporin A interfered with CD95L expression, Ascorbic Acid and Glutathione inhibited cell death triggered by CD95/CD95L interaction; Genistein and PNU152518 acted on both steps. The occurrence of oxidative stress during CD95-dependent apoptosis was supported by the direct evidence of ROI production.

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Glutathione deficiency and HIV

Cited by 18 publications

References 2 publications

N-Acetylcysteine: Potential for AIDS Therapy

N-Acetylcysteine: Potential for AIDS Therapy

Identification of Two Rat Genes Orthologous to the Human Interleukin-8 Receptors

Apoptosis induced by HIV‐gp120 in a Th1 clone involves the generation of reactive oxygen intermediates downstream CD95 triggering

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