Antiapoptotic and antigenotoxic effects of N-acetylcysteine in human cells of endothelial origin

N-Acetylcysteine (NAC) is a drug bearing multiple preventive properties that can inhibit genotoxicity and carcinogenicity. NAC also inhibits invasion and metastasis of malignant cells, as well as tumor take. We recently demonstrated the effects of NAC on Kaposi's sarcoma cells supernatant-induc...

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Bibliographic Details
Published inAnticancer research Vol. 20; no. 5A; p. 3183
Main Authors Aluigi, M G, De Flora, S, D'Agostini, F, Albini, A, Fassina, G
Format Journal Article
LanguageEnglish
Published Greece 01.09.2000
Subjects
Acetylcysteine - pharmacology
Angiogenesis Inhibitors - pharmacology
Antimutagenic Agents - pharmacology
Apoptosis - drug effects
Buthionine Sulfoximine - pharmacology
Cell Line
Endothelium, Vascular - drug effects
Humans
Paraquat - antagonists & inhibitors
Paraquat - pharmacology
Transforming Growth Factor beta - pharmacology
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Summary:N-Acetylcysteine (NAC) is a drug bearing multiple preventive properties that can inhibit genotoxicity and carcinogenicity. NAC also inhibits invasion and metastasis of malignant cells, as well as tumor take. We recently demonstrated the effects of NAC on Kaposi's sarcoma cells supernatant-induced invasion in vitro and angiogenesis in vivo. Many anticancer agents act through cytotoxicity of rapidly proliferating cells and several antineoplastic drugs induce apoptosis of cancer cells. Since endothelial cells are the target for the inhibition of angiogenesis, we wanted to verify that NAC, while inhibiting tumor vascularization and endothelial cell invasion would not induce endothelial cell apoptosis. We tested the ability of NAC to modulate apoptosis and cytogenetic damage in vitro and to promote differentiation on a reconstituted basement membrane (matrigel) in two endothelial cell lines (EAhy926 and HUVE). Treatment with NAC protected endothelial cells from TGF-beta-induced apoptosis and paraquat-induced cytogenetic damage. Therefore, NAC acts as an antiangiogenic agent and, at the same time, appears to prevent apoptosis and oxygen-related genotoxicity in endothelial cells.
ISSN:0250-7005