Effect of sodium selenite on lipids and lipid‐metabolizing enzymes in N‐nitrosodiethylamine‐induced hepatoma‐bearing rats

Abstract

As part of a substantial effort to curtail the adverse health effects posed by hepatoma, studies have been conducted to elucidate the possible mechanism for the anticarcinogenic action of sodium selenite against N-nitrosodiethylamine-induced hepatoma. Several investigations recognize selenium as potent antioxidant, as well as an anticarcinogen, in both animal and human systems. Sodium selenite was administered to Wistar rats bearing hepatoma induced by N-nitrosodiethylamine to study the alterations in the concentration of lipid profiles and in activities of some lipid-metabolizing enzymes. Control and tumor-bearing animals were fed 4 ppm of sodium selenite before initiation or during initiation and/or during promotion phases of carcinogenesis. Hepatic total cholesterol, free cholesterol, triglycerides, free fatty acids, and phospholipids were significantly lowered, whereas cholesterol esters was greater because of selenite administration in N-nitrosodiethylamine-induced tumor-bearing rats. Total lipase, lipoprotein lipase, lecithin: cholesterol acyl transferase, and cholesterol ester synthetase registered greater activities in hepatoma of selenite administered rats with tumor whereas the activity of cholesterol ester hydrolase in hepatoma-bearing animals was lower as a result of selenite administration. These observations clearly indicate the effect of selenite in correcting the abnormalities of lipid metabolism in tumor-induced animals. Previous evidence from this laboratory and present observations it can be concluded that the anticancer property of selenite my also be by its strong hypolipidemic capacity in vivo system.

Pharmacologic and genetic inhibition of cholesterol esterification reduces tumour burden: a pan-cancer systematic review and meta-analysis of preclinical models

“…Conversely, high LCAT expression is associated with improved prognosis for liver cancer patients [14] and is often lower in liver cancer than normal tissue in humans [15] and rat models [16][17][18]. At the molecular level, cholesteryl esters promote cancer proliferation and invasiveness [19] and thus SOATs were considered as promising targets and the anticancer action of natural SOAT inhibitors such as auraptene and bryonolic acid was elucidated [20,21].…”