High α-tocopherol dosing increases lipid metabolism by changing redox state in damaged rat gastric mucosa and liver after ethanol treatment

Abstract

Regeneration of ethanol-injured rat gastric mucosa must undergo changes in major metabolic pathways to achieve DNA replication and cell proliferation. These events are highly dependent on glucose utilization and inhibited by vitamin E (VE) (α-tocopherol) administration. Therefore, the present study aimed at assessing lipid metabolism in the gastric mucosa and ethanol-induced gastric damage and the effect of α-tocopherol administration. For this, rates of fatty acid β-oxidation and lipogenesis were tested in gastric mucosa samples. Through histological analysis, we found loss of the mucosa's superficial epithelium, which became gradually normalized during the recovery period. Proliferation of gastric mucosa occurred with augmented formation of β-oxidation by-products, diminished synthesis of triacylglycerols (TGs), as well as of phospholipids, and a reduced cytoplasmic NAD/NADH ratio, whereas the mitochondrial redox NAD/NADH ratio was much less affected. In addition, α-tocopherol increased palmitic acid utilization in the gastric mucosa, which was accompanied by the induction of 'mirror image' effects on the cell redox state, reflected in an inhibited cell gastric mucosa proliferation by the vitamin administration. In conclusion, the present study shows, for the first time, the role of lipid metabolism in the adaptive cell gastric mucosa changes that drive proliferation after a chronic insult. Moreover, α-tocopherol increased gastric mucosa utilization of palmitic acid associated with energy production. These events could be associated with its antioxidant properties in co-ordination with regulation of genes and cell pathways, including changes in the cell NAD/NADH redox state.

Theaflavins attenuate ethanol‑induced oxidative stress and cell apoptosis in gastric mucosa epithelial cells via downregulation of the mitogen‑activated protein kinase pathway

“…It is well established that chronic alcohol consumption is one of the most important risk factors for the induction of digestive tract diseases ( 37 ). Chronic, excessive alcohol consumption may lead to the induction of various acute digestive tract diseases, including gastritis, gastric ulcers and gastrorrhagia, as a result of subsequent gastric mucosa injury, particularly via oxidative stress and apoptosis ( 38 , 39 ).…”

Interaction between and impact of IL‐6 genotype and alpha‐tocopherol levels on periodontal condition in aging individuals

“…Moreover, α‐tocopherol is known to induce the utilization of palmitic acid, which is related to energy production, by the gastric mucosa. These events could be related to the antioxidant properties of α‐tocopherol in cooperation with gene and cellular pathway control, such as changes in the cell's NAD/NADH redox state 37 . Vitamin E has been shown to play an important role in the adjustment of signal transduction and gene expression pathways for adequate intake, distribution, metabolism, and molecular action; if these actions are impaired, the physiological and pathophysiological cellular functions that aid in disease prevention are affected 38 .…”

The Role of Insulin/glucagon Ratio and Cell Redox State in the Hyperglycemia Induced by Exposure to Pulsed Electromagnetic Fields in Rats

“…For this, total lipids were extracted from the tissue pellets with chloroform, and the neutral lipids and phospholipids were separated on silica gel thin-layer (TLC) plates. The TG fraction was revealed by staining with iodine vapors and this lipid fraction was scraped into counting vials (27).…”