title: The antiapoptotic effects of sulphurous mineral water and sodium hydrosulphide on diabetic rat testes.
abstract: OBJECTIVE
  It is well known that diabetes mellitus is associated with the impairment of testicular function. In the present study, we aimed to study the effects of sulphurous mineral water or sodium hydrosulphide (NaHS) on apoptotic testicular damage in rats with streptozotocin (STZ)-induced diabetes.
  
  
  METHODS
  Sulphurous mineral water (as drinking water) or NaHS (14 μmol/kg body weight/day, I.P.) was administered for 7 wks to rats with STZ-induced diabetes.
  
  
  RESULTS
  Hyperglycaemia, an overproduction of glycated haemoglobin (HbA1C) and a decline in serum insulin, C-peptide and insulin-like growth factor-I (IGF-I) were observed in diabetic rats. A decline in the serum testosterone level and an impairment of spermatogenesis, as indicated by a histopathological examination of diabetic rats, demonstrated significant testicular damage. Sulphurous mineral water and NaHS treatment may have improved the level of testicular GSH by blocking the overexpression of some apoptosis-related regulatory proteins such as Bax/Bcl-2, cytochrome c, caspase-9 and -3, and p53. This anti-apoptotic potential was associated with an increase in serum testosterone level and the amelioration of hyperglycaemia-related biochemical parameters. The histopathological examination was in harmony with the biochemical and molecular findings.
  
  
  CONCLUSIONS
  Our study provides the first indication that sulphurous mineral water and NaHS may have a novel anti-apoptotic potential that could be a useful treatment in preventing diabetes-induced testicular dysfunction.
authors.affiliation: Biochemistry Department, Faculty of Pharmacy, Cairo University, Cairo, Egypt. nerminsadik@yahoo.com
authors.forename: Nermin A H
authors.initials: NA
authors.lastname: Sadik
authors.forename: Mohamed M
authors.initials: MM
authors.lastname: El-Seweidy
authors.forename: Olfat G
authors.initials: OG
authors.lastname: Shaker
mesh_terms: D000818:Animals; D000903:Antibiotics, Antineoplastic / Q000633:toxicity; D017209:Apoptosis / Q000187:drug effects*; D002096:C-Peptide / Q000378:metabolism; D053148:Caspase 3 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D045304:Cytochromes c / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D006442:Glycated Hemoglobin / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000494:pharmacology / Q000627:therapeutic use; D007328:Insulin / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D008297:Male; D008900:Mineral Waters / Q000627:therapeutic use*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013091:Spermatogenesis / Q000187:drug effects; D013311:Streptozocin / Q000633:toxicity; D013440:Sulfides / Q000627:therapeutic use*; D013455:Sulfur / Q000737:chemistry / Q000494:pharmacology*; D013737:Testis / Q000187:drug effects*; D013739:Testosterone / Q000097:blood; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D000903:Antibiotics, Antineoplastic; D002096:C-Peptide; D053148:Caspase 3; D053453:Caspase 9; D045304:Cytochromes c; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin; D007334:Insulin-Like Growth Factor I; D008900:Mineral Waters; D019253:Proto-Oncogene Proteins c-bcl-2; D013311:Streptozocin; D013440:Sulfides; D013455:Sulfur; D013739:Testosterone; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein; C025451:sodium bisulfide