title: Prevention of immune dysfunction and vitamin E loss by dehydroepiandrosterone and melatonin supplementation during murine retrovirus infection.
abstract: Female C57BL/6 mice infected with the LP-BM5 leukaemia retrovirus developed murine acquired immune-deficiency syndrome (AIDS). Dehydroepiandrosterone (DHEA) and melatonin (MLT) modify immune dysfunction and prevent lipid peroxidation. We investigated whether DHEA and MLT could prevent immune dysfunction, excessive lipid peroxidation, and tissue vitamin E loss induced by retrovirus infection. Retrovirus infection inhibited the release of T helper 1 (Th1) cytokines, stimulated secretion of Th2 cytokines, increased hepatic lipid peroxidation, and induced vitamin E deficiency. Treatment with DHEA or MLT alone, as well as together, largely prevented the reduction of B- and T-cell proliferation as well as of Th1 cytokine secretion caused by retrovirus infection. Supplementation also suppressed the elevated production of Th2 cytokines stimulated by retrovirus infection. DHEA and MLT simultaneously reduced hepatic lipid peroxidation and prevented vitamin E loss. The use of DHEA plus MLT was more effective in preventing retrovirus-induced immune dysfunction than either DHEA or MLT alone. These results suggest that supplementation with DHEA and MLT may prevent cytokine dysregulation, lipid oxidation and tissue vitamin E loss induced by retrovirus infection. Similarly, hormone supplementation also modified immune function and increased tissue vitamin E levels in uninfected mice.
authors.affiliation: Arizona Prevention Center, University of Arizona, Tucson, AZ 85724, USA.
authors.forename: Z
authors.initials: Z
authors.lastname: Zhang
authors.forename: M
authors.initials: M
authors.lastname: Araghi-Niknam
authors.forename: B
authors.initials: B
authors.lastname: Liang
authors.forename: P
authors.initials: P
authors.lastname: Inserra
authors.forename: S K
authors.initials: SK
authors.lastname: Ardestani
authors.forename: S
authors.initials: S
authors.lastname: Jiang
authors.forename: S
authors.initials: S
authors.lastname: Chow
authors.forename: R R
authors.initials: RR
authors.lastname: Watson
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D001402:B-Lymphocytes / Q000473:pathology; D002455:Cell Division / Q000187:drug effects; D002784:Cholesterol / Q000032:analysis / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D003687:Dehydroepiandrosterone / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D005260:Female; D015227:Lipid Peroxidation; D008099:Liver / Q000737:chemistry / Q000378:metabolism; D008550:Melatonin / Q000627:therapeutic use*; D051379:Mice; D008810:Mice, Inbred C57BL; D016183:Murine Acquired Immunodeficiency Syndrome / Q000188:drug therapy / Q000276:immunology / Q000821:virology*; D010743:Phospholipids / Q000032:analysis / Q000378:metabolism; D012192:Retroviridae Infections / Q000188:drug therapy / Q000276:immunology*; D013601:T-Lymphocytes / Q000473:pathology; D018417:Th1 Cells / Q000378:metabolism; D018418:Th2 Cells / Q000378:metabolism; D014810:Vitamin E / Q000032:analysis / Q000378:metabolism*
chemical_list: D000975:Antioxidants; D016207:Cytokines; D010743:Phospholipids; D014810:Vitamin E; D003687:Dehydroepiandrosterone; D002784:Cholesterol; D008550:Melatonin