Urea cycle enzymes expression level in liver following sleep deprivation in male rats

Sleep is essential for maintaining metabolic balance and normal organ function. Sleep loss is known to impair physiological systems, including the liver, a central organ for nitrogen metabolism and the urea cycle. This study examined the effects of chronic sleep deprivation on biochemical indices, urea cycle gene expression, and liver histology in an experimental rat model.

Male Wistar rats were randomized into two groups: Sleep deprivation (SD) and control. Sleep deprivation was induced for three days using a treadmill device with cycles of 30 s on/90 s off. On the fourth day, animals were anesthetized, and blood and liver samples were collected. Serum biochemical markers (BUN, ALT, AST, ALP) were quantified. Gene expression of ASS, ASL, and ARG1 was analyzed, and liver histology was assessed by hematoxylin and eosin (H&E) staining. Statistical comparisons were performed using appropriate tests.

Chronic sleep deprivation significantly elevated serum BUN levels compared with controls (P < 0.01). ALT and AST levels increased significantly (P < 0.05 and P < 0.01, respectively), while ALP increased at P < 0.05. Hepatic expression of ASS, ASL, and ARG1 was significantly downregulated (P < 0.01). No histological alterations were detected in liver tissue.

Short-term sleep deprivation increases biochemical markers of hepatic injury and suppresses expression of key urea cycle genes, although without detectable histological changes. These findings emphasize the importance of adequate sleep in preserving hepatic nitrogen metabolism. Future studies with longer deprivation periods and additional markers (oxidative stress, inflammation, hormones) are needed to clarify the underlying mechanisms.