Hepatic ischemia-reperfusion injury is a common complication of liver surgery and transplantation. The morbidity related to hepatic surgery under a total vascular exclusion or following liver transplantation is caused by ischemia-reperfusion damage. Numerous pathways are involved in the pathophysiology of hepatic ischemia-reperfusion, and they all play a role in the overall injury to varying degrees. Post-surgical hepatic dysfunction is one of the primary causes of morbidity and mortality. Several studies have suggested oxidative stress, inflammation, mitochondrial dysfunction, activation of the liver Kupffer cell, overexpression of Vascular Cell Adhesion Molecule, and facilitation of (PMN) polymorphonuclear neutrophil damage are involved in the pathophysiology of ischemia-reperfusion damage in the liver. Ornithine is an amino acid and non-proteinogenic in nature. It plays a vital role in the urea cycle. Ornithine is commonly present in dietary supplements that have been proven to influence the hepatic ischemia-reperfusion injury-linked pathways, hence lowering deterioration in the liver ischemia/reperfusion dysfunction. Liver cirrhosis has been treated using a stable salt of ornithine and aspartic acid. After surgical tumour removal, patients who take ornithine aspartate may experience less hepatic ischemia-reperfusion damage. Lornithine functions as a precursor to citrulline and arginine and enables the elimination of extra nitrogen. Ischemia/reperfusion injury is caused by the aggravation of cellular upsets and mortality following the refurbishment of blood flow to the earlier ischemic tissue. This article confers a deep understanding of the protective effects of ornithine on hepatic ischemia/reperfusion injury as well as evidence linking ornithine's function tending towards the detoxification mechanism of the liver.