title: Prevention of arsenic-mediated reproductive toxicity in adult female rats by high protein diet.
abstract: BACKGROUND
  The detrimental effects of arsenic on female reproductive functions may involve overt oxidative stress. Casein and pea [Pisum sativum Linn. (Fabaceae)] proteins have antioxidant properties.
  
  
  OBJECTIVE
  To investigate the role of casein- and pea-supplemented high-protein diet (HPD) in utero-ovarian protection from arsenic toxicity.
  
  
  METHODS
  Adult female Wistar rats were orally gavaged with vehicle (Gr-I) or arsenic at 3 ppm/rat/d (Gr-II and Gr-III) for 30 consecutive days, when they were maintained on either regular diet containing 18% protein (Gr-I and Gr-II), or HPD containing 27% protein in the form of casein (20%) and pea (7%) (Gr-III). Reproductive functions were evaluated using a battery of biochemical and histological techniques.
  
  
  RESULTS
  As compared to Gr-I, the Gr-II rats suffered from loss of estrous cyclicity, reduction in weight (mg/100 g body weight) of ovary (Gr-I: 54.3 ± 4.2 versus Gr-II: 35.8 ± 1.6; p < 0.001) and uterus (Gr-I: 161.7 ± 24.6 versus Gr-II: 94.44 ± 13.2; p < 0.05), utero-ovarian degeneration, attenuated ovarian activities (unit/mg tissue/h) of Δ(5), 3β-hydroxysteroid dehydrogenase (Gr-I: 3.41 ± 0.12 versus Gr-II: 2.31 ± 0.09; p < 0.01) and 17β-hydroxysteroid dehydrogenase (Gr-I: 3.82 ± 0.57 versus Gr-II: 1.24 ± 0.19; p < 0.001), and decreased serum estradiol level (pg/ml) (Gr-I: 61.5 ± 2.06 versus 34.1 ± 2.34; p < 0.001). Ovarian DNA damage was preponderant with blatant generation of malondialdehyde (nM/mg tissue; Gr-I: 15.10 ± 2.45 versus Gr-II: 29.51 ± 3.44; p < 0.01) and attenuated superoxide dismutase activity (unit/mg tissue) (Gr-I: 2.18 ± 0.19 versus Gr-II: 1.33 ± 0.18; p < 0.05). The Gr-III rats were significantly protected from these ill effects of arsenic.
  
  
  CONCLUSIONS
  HPD, by way of antioxidant properties, may find prospective role in the protection of reproductive damage caused by arsenic.
authors.affiliation: Department of Physiology, Presidency University , Kolkata , India .
authors.forename: Srabanti
authors.initials: S
authors.lastname: Mondal
authors.forename: Sanjit
authors.initials: S
authors.lastname: Mukherjee
authors.forename: Keya
authors.initials: K
authors.lastname: Chaudhuri
authors.forename: Syed N
authors.initials: SN
authors.lastname: Kabir
authors.forename: Prabir
authors.initials: P
authors.lastname: Kumar Mukhopadhyay
mesh_terms: D015067:17-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D015096:3-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D000821:Animal Feed; D000818:Animals; D000077237:Arsenic Trioxide; D001152:Arsenicals; D001835:Body Weight; D002364:Caseins / Q000008:administration & dosage*; D019610:Cytoprotection; D004249:DNA Damage; D004435:Eating; D004785:Environmental Pollutants / Q000633:toxicity*; D004958:Estradiol / Q000097:blood; D030762:Estrous Cycle / Q000187:drug effects; D005260:Female; D008315:Malondialdehyde / Q000378:metabolism; D009929:Organ Size; D010053:Ovary / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D018384:Oxidative Stress; D010087:Oxides / Q000633:toxicity*; D018532:Pisum sativum; D014674:Plant Proteins, Dietary / Q000008:administration & dosage*; D051381:Rats; D017208:Rats, Wistar; D012098:Reproduction / Q000187:drug effects*; D013482:Superoxide Dismutase / Q000378:metabolism; D014599:Uterus / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology
chemical_list: D001152:Arsenicals; D002364:Caseins; D004785:Environmental Pollutants; D010087:Oxides; D014674:Plant Proteins, Dietary; D004958:Estradiol; D008315:Malondialdehyde; D015067:17-Hydroxysteroid Dehydrogenases; D015096:3-Hydroxysteroid Dehydrogenases; D013482:Superoxide Dismutase; D000077237:Arsenic Trioxide