N-acetylcysteine: potential for AIDS therapy.
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.
Roederer
M
M
Department of Genetics, Stanford University, Calif. 94305.
Staal
F J
FJ
Ela
S W
SW
Herzenberg
L A
LA
Herzenberg
L A
LA
D000111:Acetylcysteine / Q000494:pharmacology / Q000627:therapeutic use*; D000163:Acquired Immunodeficiency Syndrome / Q000188:drug therapy* / Q000378:metabolism; D016207:Cytokines / Q000097:blood; D004359:Drug Therapy, Combination; D005978:Glutathione / Q000378:metabolism*; D015658:HIV Infections / Q000188:drug therapy* / Q000378:metabolism; D006801:Humans; D007249:Inflammation; D008214:Lymphocytes / Q000276:immunology / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism
D016207:Cytokines; D017382:Reactive Oxygen Species; D005978:Glutathione; D000111:Acetylcysteine