In rats exposed to stressful foot shocks, the peptide Semax helped protect the liver at higher doses (50 and 450 µg/kg) by lowering a marker of fat damage (MDA) and reducing stress‑related liver enzyme spikes. Lower doses (5 and 150 µg/kg) actually increased the damage marker. Over longer‑term stress, Semax improved liver protein‑making function and lowered another liver enzyme (ALT), but didn’t strongly affect the fat‑damage marker.

The effect of ACTH4-7-PGP (Semax) intraperitoneal injection at the doses of 5, 50, 150 and 450 μg/kg b. w. on lipid peroxidation and functional hepatocytes state in Wistar male rats subjected to acute and chronic electrical foot-shock stress was investigated. It was observed that peptide at the doses of 50 and 450 μg/kg normalized malondialdehyde (MDA) level elevation in the liver homogenate caused by acute foot-shock stress. On the contrary, at the doses of 5 and 150 μg/kg Semax significantly increased MDA content without essential changes of antioxidant defense activity (catalase, superoxide dismutase, common antioxidative activity). In serum peptide at the all doses decreased stress-induced asparate aminotransferase activity elevation. In chronic stress peptide provided the normalization of protein synthetic hepatocytes function and the serum alanine aminotransferase activity with less effect on lipid peroxidation.