Human immunodeficiency virus type-1 coat glycoprotein gp 120 causes delayed programmed cell death (apoptosis) in rat brain neocortex. Here, we investigated the possible role of the arachidonate cascade and membrane peroxidation in this process. It is shown that gp 120 causes a rapid increase in the activity and expression of the arachidonate-metabolizing enzyme prostaglandin H synthase, paralleled by increased prostaglandin E(2) levels. The selective inhibitor of prostaglandin H synthase indomethacin inhibited enzyme activity, reduced prostaglandin E(2) content, and partially protected neocortex against gp 120-induced apoptosis. Conversely, the activity and expression of the arachidonate-metabolizing enzyme 5-lipoxygenase decreased upon gp 120 treatment, as well as the level of its product, leukotriene B(4). Treatment with gp 120 also reduced membrane lipid peroxidation, and this may be implicated in the execution of programmed cell death. These results suggest that early derangement of the arachidonate cascade in favor of prostanoids may be instrumental in the execution of delayed apoptosis in the brain neocortex of rats.

Maccarrone, M., Bari, M., Corasaniti, M., Nistico', R.g., Bagetta, G., FINAZZI AGRO', A. (2000). HIV-1 coat glycoprotein gp120 induces apoptosis in rat brain neocortex by deranging the arachidonate cascade in favor of prostanoids. JOURNAL OF NEUROCHEMISTRY, 75(1), 196-203.

HIV-1 coat glycoprotein gp120 induces apoptosis in rat brain neocortex by deranging the arachidonate cascade in favor of prostanoids

MACCARRONE, MAURO;NISTICO', ROBERT GIOVANNI;BAGETTA, GIACINTO;FINAZZI AGRO', ALESSANDRO
2000-07-01

Abstract

Human immunodeficiency virus type-1 coat glycoprotein gp 120 causes delayed programmed cell death (apoptosis) in rat brain neocortex. Here, we investigated the possible role of the arachidonate cascade and membrane peroxidation in this process. It is shown that gp 120 causes a rapid increase in the activity and expression of the arachidonate-metabolizing enzyme prostaglandin H synthase, paralleled by increased prostaglandin E(2) levels. The selective inhibitor of prostaglandin H synthase indomethacin inhibited enzyme activity, reduced prostaglandin E(2) content, and partially protected neocortex against gp 120-induced apoptosis. Conversely, the activity and expression of the arachidonate-metabolizing enzyme 5-lipoxygenase decreased upon gp 120 treatment, as well as the level of its product, leukotriene B(4). Treatment with gp 120 also reduced membrane lipid peroxidation, and this may be implicated in the execution of programmed cell death. These results suggest that early derangement of the arachidonate cascade in favor of prostanoids may be instrumental in the execution of delayed apoptosis in the brain neocortex of rats.
lug-2000
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore BIO/14 - FARMACOLOGIA
English
Animals; Apoptosis; Arachidonate 5-Lipoxygenase; Arachidonic Acid; Cyclooxygenase Inhibitors; Dinoprostone; HIV Envelope Protein gp120; Indomethacin; Injections, Intraventricular; Leukotriene B4; Lipid Peroxidation; Male; Neocortex; Prostaglandin-Endoperoxide Synthases; Prostaglandins; Rats; Rats, Wistar
Maccarrone, M., Bari, M., Corasaniti, M., Nistico', R.g., Bagetta, G., FINAZZI AGRO', A. (2000). HIV-1 coat glycoprotein gp120 induces apoptosis in rat brain neocortex by deranging the arachidonate cascade in favor of prostanoids. JOURNAL OF NEUROCHEMISTRY, 75(1), 196-203.
Maccarrone, M; Bari, M; Corasaniti, M; Nistico', Rg; Bagetta, G; FINAZZI AGRO', A
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Descrizione: HIV-1 coat glycoprotein gp120 induces apoptosis in rat brain neocortex by deranging the arachidonate cascade in favor of prostanoids
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/133254
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