title: Androgen deprivation by flutamide modulates uPAR, MMP-9 expressions, lipid profile, and oxidative stress: amelioration by daidzein.
abstract: The growth and development of prostate gland is governed by testosterone. Testosterone helps in maintaining the adipose tissue stores of the body. It is well documented that with advancing age there has been a gradual decline in testosterone levels. Our aim was to study the protective role of daidzein on flutamide-induced androgen deprivation on matrix degrading genes, lipid profile and oxidative stress in Wistar rats. Sub-chronic (60 days) flutamide (30 mg/kg b.wt) administration resulted in marked increase in expressions of matrix degrading genes [matrix metalloproteases 9 and urokinase plasminogen activation receptor]. Additionally, it increased the levels of low density lipoproteins, total cholesterol, triglycerides, and lowered the levels of high density lipoproteins and endogenous antioxidant levels. Oral administration of daidzein (20 and 60 mg/kg b.wt) restituted the levels to normal. Daidzein administration resulted in amelioration of the prostate atrophy, degeneracy and invasiveness induced by flutamide. Our findings suggest that the daidzein may be given as dietary supplement to patients who are on androgen deprivation therapy, to minimize the adverse effects related to it and also retarding susceptibility of patients to cardiovascular diseases.
authors.affiliation: Molecular Carcinogenesis and Chemoprevention Division, Department of Medical Elementology and Toxicology, Faculty of Science, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi, 110 062, India.
authors.forename: Abdul
authors.initials: A
authors.lastname: Lateef
authors.forename: Abdul Quaiyoom
authors.initials: AQ
authors.lastname: Khan
authors.forename: Mir
authors.initials: M
authors.lastname: Tahir
authors.forename: Rehan
authors.initials: R
authors.lastname: Khan
authors.forename: Muneeb U
authors.initials: MU
authors.lastname: Rehman
authors.forename: Farrah
authors.initials: F
authors.lastname: Ali
authors.forename: Oday O
authors.initials: OO
authors.lastname: Hamiza
authors.forename: Sarwat
authors.initials: S
authors.lastname: Sultana
mesh_terms: D000726:Androgen Antagonists / Q000008:administration & dosage; D000818:Animals; D001284:Atrophy / Q000188:drug therapy; D002374:Catalase / Q000378:metabolism; D002784:Cholesterol / Q000096:biosynthesis; D005485:Flutamide / Q000008:administration & dosage; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D007529:Isoflavones / Q000494:pharmacology*; D050356:Lipid Metabolism / Q000187:drug effects*; D008055:Lipids / Q000096:biosynthesis*; D008075:Lipoproteins, HDL / Q000096:biosynthesis; D008077:Lipoproteins, LDL / Q000096:biosynthesis; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism*; D009919:Orchiectomy; D018384:Oxidative Stress / Q000187:drug effects; D048789:Phytoestrogens / Q000494:pharmacology; D011467:Prostate / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D055293:Receptors, Urokinase Plasminogen Activator / Q000378:metabolism*; D014280:Triglycerides / Q000096:biosynthesis
chemical_list: D000726:Androgen Antagonists; D007529:Isoflavones; D008055:Lipids; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D048789:Phytoestrogens; D055293:Receptors, Urokinase Plasminogen Activator; D014280:Triglycerides; C004742:daidzein; D005485:Flutamide; D002784:Cholesterol; D002374:Catalase; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; D020780:Matrix Metalloproteinase 9; D005978:Glutathione