Crotonaldehde oral exposure disrupt cardiac energy metabolism and induces oxidative stress via down-regulation of nrf-2 and up-regulation of PPARα

Abstract

Alterations in cardiac energy metabolic pathways have been linked to cardiac dysfunction. This study investigated cardiac energy metabolism in male rats exposed to crotonaldehyde. Thirty-six male Wistar rats (150–170 g; n = 9) were grouped into 4 (I-IV): Control (normal saline 10 mL/kg), crotonaldehyde (0.75, 1.5, and 2.5 mg/kg, p.o) for 28 days. Levels of creatinine-kinase-myocardial-band, cardiac-troponin-I, glucose increased significantly, while triglyceride, free-fatty-acid, and insulin reduced significantly in all groups compared with control. Cardiac Pyruvate level, hexokinase and pyruvate dehydrogenase activities increased significantly in all crotonaldehyde-treated groups compared with control. Cardiac levels of malondialdehyde and hydrogen-peroxide increased significantly, while glutathione and nuclear-factor-erythroid-2-related-factor-2 reduced; superoxide-dismutase and catalase activities decreased following crotonaldehyde exposure compared with control. Cardiac glucose-transporter-4 and peroxisome-proliferator-activated-receptor-alpha expression increased in groups III and IV, while carnitine-palmitoyltransferase1β expression decreased in group II but increased in groups III and IV compared with control. Crotonaldehyde exposure exerts cardio-toxic effects by altering cardiac energy metabolism.