Thirayudh glinsukonChaivat ToskulkaoThyon ChentanezRachada Stitmetakul2024-07-052024-07-05199319932024Thesis (M.Sc. (Physiology))--Mahidol University, 1993https://repository.li.mahidol.ac.th/handle/20.500.14594/99338Physiology (Mahidol University 1993)In the study of the effect of endurance training in adult male Wistar rats, it was found that after 14 wk swim training program (30 min/day, 5 days/wk with 1% BW resistance, training induced physiological and biochemical adaptation as shown by reduction in final body weight (12%), increase in relative heart weight (30%), decrease in resting heart rate (13%) in addition to increase in the activities of succinic dehydrogenase (49%) and citrate synthase (136%) in gastrocnemius muscle. Training also produced increase in CAT activity and decrease in lipid peroxide level in muscle, but did not alter in GPX and GST activity as well as GSH. In trained rats, these changes were not seen in the liver and heart. Furthermore, SGOT and SGPT activity were not affected. These data suggested that endurance training can result in reduction in lipid peroxide level in muscle. It. is possible that activation of CAT and increase in respiratory capacity were contributory factors responsible for regulating lipid peroxidation after training. In the study of effect of endurance training pretreatment on AFB1 hepatotoxicity, the rats were trained for 14 wk according to exercise training prograrn then followed by a single intraperitoneal administration of AFB1 (2 mg/kg BW). The hepatotoxicity and the detoxifying systems changes were determined at 0, 12, 24 hours after AFB1 dosing. It was demonstrated that endurance training pretreatment enhanced hepatotoxicity, as shown by more increase in SGOT (1.8 fold) and SGPT (8 fold) activity, at 2 so reduced in the activities of CAT, GPX, and GST as well as GSH content at 12-Z4 h after AFB1 administration. However, lipid peroxide level was decreased to control level at 24 h. It was concluded that endurance training pretreatment may play a role in increasing of AFB1 metabolism and lowering detoxifying systems in particular reference to GSH conjugation. The mechanism by which AFB1 treatment induced hepatotoxicity may not related to the lipid peroxidation produced in trained rats.xi, 175 leaves : ill.application/pdfengผลงานนี้เป็นลิขสิทธิ์ของมหาวิทยาลัยมหิดล ขอสงวนไว้สำหรับเพื่อการศึกษาเท่านั้น ต้องอ้างอิงแหล่งที่มา ห้ามดัดแปลงเนื้อหา และห้ามนำไปใช้เพื่อการค้าAflatoxin B1ExerciseLipid PeroxidesPhysical enduranceMaster ThesisMahidol University