title: Response of anti-oxidant enzymes mRNA in the neonatal rat liver exposed to 1,2,3,4-tetrachlorodibenzo-p-dioxin via lactation.
abstract: BACKGROUND
  The aim of this study was to assess the response to dioxin-induced oxidative stress in neonates via lactation in the model we have described previously.
  
  
  METHODS
  Maternal rats were treated with a single dose of 50 or 100 micro mol/kg 1,2,3,4-tetrachlorodibenzo-p-dioxin (TCDD) on the first day postpartum (day 1). Messenger RNA levels of the key anti-oxidant enzymes (AOE), phospholipid hydroperoxide-glutathione peroxidase (PH-GPx), cellular-glutathione peroxidase (cell-GPx), copper-zinc superoxide dismutase (CuZn SOD), manganese superoxide dismutase (Mn SOD) and catalase (CAT) in the neonatal and maternal livers were determined by a competitive reverse transcription- polymerase chain reaction method.
  
  
  RESULTS
  Lactational transfer of 1,2,3,4-TCDD induced an inhibition of PH-GPx and cell-GPx mRNA in the neonatal liver on day 2 to 68 (P < 0.01) and 62% (P < 0.05) of the control at 100 micro mol/kg, respectively. Both GPx mRNA returned to control levels on day 6 and thereafter increased to levels higher than the controls on day 10. In the dam rat, 10 days after the treatment, no remarkable change of PH-GPx or cell-GPx mRNA was observed. Copper-zinc superoxide dismutase and CAT mRNA of neonates on day 2 were also suppressed at 100 micro mol/kg and then slightly increased on day 10. However, Mn SOD mRNA was not suppressed, but increased to a 2.1-fold level of the control (P < 0.05) on day 10 with 100 micro mol/kg 1,2,3,4-TCDD.
  
  
  CONCLUSIONS
  Quantitative analysis of AOE mRNA showed that PH-GPx and cell-GPx mRNA, as well as CuZn SOD and CAT mRNA in the neonatal liver were suppressed for a short period of time by 1,2,3,4-TCDD exposure via lactation. Dioxin induced oxidative stress by lactational transfer may alter pretranslation regulation of protective AOE in neonates.
authors.affiliation: Department of Pediatrics, Tottori University, Yonago, Japan. ykono@boshi.twmu.ac.jp
authors.forename: Yumi
authors.initials: Y
authors.lastname: Kono
authors.forename: Shin'Ichi
authors.initials: S
authors.lastname: Okada
authors.forename: Yusaku
authors.initials: Y
authors.lastname: Tazawa
authors.forename: Susumu
authors.initials: S
authors.lastname: Kanzaki
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Mura
authors.forename: Etsuko
authors.initials: E
authors.lastname: Ueta
authors.forename: Eiji
authors.initials: E
authors.lastname: Nanba
authors.forename: Yuzuru
authors.initials: Y
authors.lastname: Otsuka
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D006224:Cricetinae; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D007774:Lactation; D015227:Lipid Peroxidation; D008099:Liver / Q000187:drug effects*; D018384:Oxidative Stress; D000072317:Polychlorinated Dibenzodioxins / Q000633:toxicity*; D011247:Pregnancy; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D000072317:Polychlorinated Dibenzodioxins; D012333:RNA, Messenger; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase