Effect of retinyl acetate on transglutaminase 2 activity in carcinogen treated rat liver.


Aydin O., Akyuz F., Tekin N., Ustuner M. C., DEĞİRMENCİ İ., Burukoglu D., ...Daha Fazla

Biotechnic & histochemistry : official publication of the Biological Stain Commission, cilt.91, sa.5, ss.342-51, 2016 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 91 Sayı: 5
  • Basım Tarihi: 2016
  • Doi Numarası: 10.3109/10520295.2016.1170879
  • Dergi Adı: Biotechnic & histochemistry : official publication of the Biological Stain Commission
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.342-51
  • Anahtar Kelimeler: carcinogen, liver, rat, retinyl acetate, transglutaminase 2, OXIDATIVE STRESS, TISSUE TRANSGLUTAMINASE, HYDROCARBON RECEPTOR, METABOLISM, RETINOIDS, EXPOSURE, CYP1A2, ENZYME, DIOXIN
  • Eskişehir Osmangazi Üniversitesi Adresli: Evet

Özet

Transglutaminase 2 (TG2) has been implicated in wound healing, cellular differentiation, apoptosis and cell survival. TG2 activity increases following acute and chronic liver injury; however, the role of TG2 in tumors, is controversial. TG2 is a retinoid-inducible enzyme. We investigated the effects of retinyl acetate (RA) on the activity and levels of TG2 during the initiation and promotion stages of liver cancer. p-Dimethylaminoazobenzene (p-DAB) was used as initiator and 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) was used as promoter in our model of carcinogenesis. Rats were divided into four groups of 24: control, corn oil control, p-DAB + TCDD, and p-DAB + TCDD + RA. Six rats from each group were sacrificed at days 30, 60, 90 and 120. TG2 activity decreased in the p-DAB + TCDD treated group, but TG2 immunostaining scores did not change by days 90 and 120. Neither TG2 enzyme activity nor the immunostaining score of TG2 protein changed in the tissues of the p-DAB + TCDD + RA group by days 90 and 120. TG2 activity was not be ameliorated by RA during the initiation or promotion stages of carcinogen induced liver cancer.