system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, DNA, Mitochondrial, Dose-Response Relationship, Drug, Energy Metabolism, Ethanol, Gastric Mucosa, Male, Malondialdehyde, Mitochondria, Mitochondrial Proton-Translocating ATPases, Models, Animal, Oxidative Stress, RNA, Messenger, Rats, Rats, Wistar, Severity of Illness Index, Thiobarbituric Acid Reactive Substances, Time Factors.
user
Does oxidative stress disturb energy metabolism of mitochondria in ethanol-induced gastric mucosa injury? Context: To study the role of mitochondrial energy disorder in the pathogenesis of ethanol-induced gastric mucosa injury. Wistar rats were used in this study. A gastric mucosal injury model was established by giving the rats alcohol. Gross and microscopic appearance of gastric mucosa and ultrastructure of mitochondria were evaluated. Malondiadehyde (MDA) in gastric mucosa was measured with thiobarbituric acid. Expression of ATP synthase (ATPase) subunits 6 and 8 in mitochondrial DNA (mtDNA) was determined by reverse transcription polymerase chain reaction (RT-PCR). The gastric mucosal lesion index was correlated with the MDA content in gastric mucosa. As the concentration of ethanol was elevated and the exposure time to ethanol was extended, the content of MDA in gastric mucosa increased and the extent of damage aggravated. The ultrastructure of mitochondria was positively related to the ethanol concentration and exposure time. The expression of mtDNA ATPase subunits 6 and 8 mRNA declined with the increasing MDA content in gastric mucosa after gavage with ethanol.
assistant
Ethanol-induced gastric mucosa injury is related to oxidative stress, which disturbs energy metabolism of mitochondria and plays a critical role in the pathogenesis of ethanol-induced gastric mucosa injury. Final Decision: yes