Immunomodulation exerted by cyclophosphamide is not interfered by N-acetyl cysteine.
Metabolism of cyclophosphamide (Cy) by liver enzymes results in cytostatic products and acrolein, which exerts urotoxicity. Experiments were designed to determine which metabolites are responsible for Cy-induced immunomodulation. For this purpose, mice were treated simultaneously with Cy and N-acetyl-cysteine (NAC), a thiol compound which reacts with acrolein, and different immunological functions were assayed. Results show that NAC did not interfere with Cy effects on antibody-dependent cellular cytotoxicity (ADCC), NK activity, delayed-type hypersensitivity (DTH) or antibody production, indicating that modulation of these functions by Cy is mediated by its cytostatic metabolites.
D000111:Acetylcysteine / Q000494:pharmacology*; D000276:Adjuvants, Immunologic; D000818:Animals; D000917:Antibody Formation / Q000187:drug effects*; D000920:Antibody-Dependent Cell Cytotoxicity / Q000187:drug effects; D003520:Cyclophosphamide / Q000494:pharmacology*; D003556:Cystitis / Q000276:immunology; D006470:Hemorrhage / Q000276:immunology; D006968:Hypersensitivity, Delayed; D007694:Killer Cells, Natural / Q000187:drug effects / Q000276:immunology; D007941:Leukemia P388 / Q000276:immunology; D008214:Lymphocytes / Q000187:drug effects / Q000276:immunology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008815:Mice, Inbred Strains
D000276:Adjuvants, Immunologic; D003520:Cyclophosphamide; D000111:Acetylcysteine