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Domínguez-Pérez, M., Nuno-Lámbarri, N., Clavijo-Cornejo, D., Luna-López, A., Souza, V., Bucio, L., Miranda, R.U., Miranda, R.U., Munoz, L., Gomez-Quiroz, L.E., Uribe-Carvajal, S. and Gutiérrez-Ruiz, M.C. (2016) Hepatocyte Growth Factor Reduces Free Cholesterol-Mediated Lipotoxicity in Primary Hepatocytes by Countering Oxidative Stress. Oxidative Medicine and Cellular Longevity, 2016, Article ID: 7960386.

has been cited by the following article:

• TITLE: Protective Effect of Ethanolamine on Hepatic Preneoplastic Alterations Induced by the Administration of N-Nitrosodiethylamine in Rats

  AUTHORS: Hajime Sasaki

  KEYWORDS: Ethanolamine, N-Nitrosodiethylamine, Protection, Hepatic lesion, Cellular Alterations

  JOURNAL NAME: Food and Nutrition Sciences, Vol.8 No.10, October 23, 2017

  ABSTRACT: The effects of exogenously administered ethanolamine (Etn) on the N-nitrosodiethylamine (NDA)-induced formation of hepatic lesions in rats were investigated. Sprague-Dawley rats were intraperitoneally administered NDA (100 mg/kg body weight) at 7-day intervals, and the animals were allowed free access to water containing Etn (15 or 50 mg/L) for 35 days. NDA-induced hepatic lesions were assessed according to the number of nodules detectable on the liver surface, areas of clear cell foci observed on histopathological thin sections, hydroxyproline levels in liver homogenates, and blood biochemical marker levels. Compared with those from control rats that were not administered Etn, livers from Etn-exposed rats had significantly fewer surface nodules and smaller areas of clear cell foci, indicating that Etn prevented or delayed the formation of preneoplastic cell alterations. Hydroxyproline levels in livers were significantly lower in Etn-treated rats, indicating that the chemical prevented the formation of fibrotic alterations. The protective effects of Etn on NDA-induced hepatic lesions were demonstrated by changes in blood biochemical marker levels. These results suggest that Etn can protect against cellular alterations induced by a carcinogenic chemical, possibly by enhancing hepatic phospholipid synthesis.