Owing to the anatomical (structural) and/or physiological (functional) alteration and dysfunction in the liver during aging, an individual can progressively lose the capability to maintain homeostasis, leading to accelerated or premature death in animals and humans.  Aging can drastically augment the vulnerability to liver injury and raise the propensity of the fibrotic response, which can increase the risk of morbidity and mortality.Hepatocellular senescence is primarily induced by oxidative stress, inflammation, apoptosis, mitochondrial dysfunction, autophagy, and alterations in the transcription/metabolic epigenome.Ames dwarf mice (exhibit a point mutation in the prophet of pit-1 gene) survive substantially longer (49–64%, males and females respectively)as compared to wild-type animals.  Ames dwarf mice are phenotypically recognized by their diminutive size and delayed puberty (due to the deficiencies in growth hormone, thyrotropin, and prolactin).At present, there is still a lack of scientific knowledge associated with the molecular mechanisms associated with the progression of aging-induced liver injury/damage.Therefore, in this study, the markers of oxidative stress, inflammation, and apoptosis were measured in the Ames dwarf mice and their age-matched controls (6 and 20 months old).  Statistical analysis was performed using Prism-V software (La Jolla, CA, USA).  The significant findings were the significant increase in serine protease activity in the liver.  Consequently, the presentfindings have highlighted the crucialrole of protease activity in the liver of growth hormone-deficient mice and may be related to their extended lifespan.