Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Zidovudine (azidothymidine, AZT), a drug used in acquired immune deficiency syndrome (AIDS), blocks reverse transcriptase and therefore inhibits human immunodeficiency virus (HIV) replication. We carried out an ultrastructural and histoenzymatic study in rat cardiac muscle. Groups of animals (3 rats per group) were given drinking water with or without AZT (1 or 2 mg AZT/ml). After 30, 60 and 120 days, the hearts were studied by light and electron microscopy. Histochemical analysis of isocitrate, succinic, malic, NADH and NADPH dehydrogenase activities revealed no changes in AZT-treated rats compared with control rats. The ultrastructural study showed a disruption of cristae and an increased size of mitochondria in rats treated with AZT for 30- and 60-days. No alterations were observed in rats that received the 120-day treatment. A statistical analysis based on electron micrographs demonstrated a time-dependent ratio between intact and disrupted mitochondria. Rats that received AZT for 30 days showed a higher number of abnormal mitochondria than rats that received the 60 day treatment. No differences with respect to rat controls were observed in the rats that received AZT for 120 days. We conclude that AZT-induced ultrastructural alterations in cardiac muscle did not modify the histochemical activity of several mitochondrial enzymes.
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PMID:Histochemical and ultrastructural changes induced by zidovudine in mitochondria of rat cardiac muscle. 753 28

We studied lumbosacral dorsal root ganglia (DRGs) from 10 patients with acquired immunodeficiency syndrome (AIDS) and five controls using immunocytochemistry, in situ hybridization and NADPH-diaphorase (NADPHd) histochemistry. Human immunodeficiency virus (HIV)-1 RNA was detected in five AIDS cases, and HIV-1 p24 antigen was found in four of these patients. The densities of nodules of Nageotte (nN), macrophages and major histocompatibility complex-class II-positive cells were significantly increased in the DRGs of AIDS patients compared to controls. Cytomegalovirus antigen was observed in the DRGs of four AIDS cases and one control, but without its presence being related to neuronal degeneration. Furthermore, we detected tumor necrosis factor, interferon-gamma, interleukin (IL)-1 beta, and IL-6 in the DRGs from AIDS patients. Using NADPHd histochemistry, we showed that the number of NADPHd-positive neurons was significantly increased in the DRGs of AIDS patients compared to controls, implying upregulation of nitric-oxide (NO) production in AIDS DRGs. Generally, there were increased numbers of nN in DRGs which contained more NADPHd-positive neurons. Additionally, immunoreactivity for an inducible form of NO synthase was detected in interstitial cells in AIDS DRGs. These results suggest that reactive inflammation, including the production of cytokines, occurs in the DRGs of AIDS patients and that excessive production of NO may be related to neuronal degeneration in AIDS DRGs.
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PMID:Increased NADPH-diaphorase reactivity and cytokine expression in dorsal root ganglia in acquired immunodeficiency syndrome. 881 58

To determine whether nitrogen monoxide (nitric oxide; NO) synthase (NOS) and NADPH diaphorase (NDP) co-containing cerebrocortical neurons (NOSN) neurons are affected in patients infected with human immunodeficiency virus type 1 (HIV-1) with and without associated intake of drugs of abuse, we examined the temporal neocortex of 24 individuals: 12 HIV-1 positive (including 3 drug users, 9 non-drug users) and 12 HIV-1 negative (including 6 drug users, and 6 non-drug users). Histochemical labeling for NDP-an enzymatic domain co-expressed in the NOS enzyme-was employed to visualize NOSN. Drug abuse and HIV-1 infection cause independently an increase in NOSN density, but combined they result in up to a 38-fold increase in NOSN density, suggesting that the combination of these factors induces NOS expression powerfully in neurons that normally do not synthesize NDP/NOS. This is associated with an increase in the proportion of NOSN displaying dystrophic changes, indicating that NOSN undergo massive degeneration in association with NOS synthesis induction. The increase in density of NOSN in HIV-1 infected drug abusers may be among the important sources of NO mediating cerebrocortical dysfunction, and the degeneration of NOS-containing local circuit neurons in patients with HIV-1 infection or drug abuse may underlie in part their neuropsychiatric manifestations.
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PMID:Increased density of neurons containing NADPH diaphorase and nitric oxide synthase in the cerebral cortex of patients with HIV-1 infection and drug abuse. 1687 97