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.

Highlights

  • 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

  • These results suggest that Etn can protect against cellular alterations induced by a carcinogenic chemical, possibly by enhancing hepatic phospholipid synthesis

  • Ethanolamine (Etn) is a nutrient synthesized from serine in vivo or supplied from food, and it is metabolized as a substrate for synthesizing phosphatidylethanolamine (PE), one of the major phospholipids constituting the mammalian cell membrane

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Summary

Introduction

Ethanolamine (Etn) is a nutrient synthesized from serine in vivo or supplied from food, and it is metabolized as a substrate for synthesizing phosphatidylethanolamine (PE), one of the major phospholipids constituting the mammalian cell membrane. Etn is phosphorylated, after which it combines with 1,2-diacylglycerol to form PE. A second pathway for synthesizing phosphatidylcholine (PC) in addition to the major pathway involving choline combining with 1,2-diacylglycerol exists; three methyl molecules provided from S-adenosylmethionine are added to the Etn moiety in PE to generate PC [5]. It was reported that Etn accelerates the proliferation of cultured cells, in which the agent promotes PE synthesis concomitantly [7]. It was reported that Etn enhances the proliferation of hepatocytes in primary culture by potentiating the action of growth factors [8] [9]. The mechanism of potentiation is unknown, one evident point is that PE and PC synthesis is apparently associated with cell growth activation by Etn in hepatocytes [10]

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