Hepatoprotective Effect of Vitamin B۱۲ in Acetaminophen Induce Hepatotoxicity in Male Rats

Acetaminophen is a pharmaceutical synthesized non-opioid analgesic that belongs to the "aniline analgesics" class of medicine. Because it lacks a significant anti-inflammatory effect, it is not classified as a non-steroidal anti-inflammatory therapeutic medication (NSAID). As an over-the-counter pain reliever and antipyretic, Acetaminophen is the active metabolite of phenacetin and acetanilide, but it is less toxic than either precursor. According to some medical studies, Acetaminophen toxicity can be treated with vitamin B۱۲. Acetaminophen-poisoned Male Wister rats were the subject model of the current study, which examines the effects of vitamin B۱۲ on their hepatic health. There were three groups of animals: Acetaminophen treated animals (۷۵۰ ml/kg), vitamin B۱۲-treated animals (۰.۶۳ g/kg), and a control group that received distilled water (۷۵۰ ml/kg). All animals were given oral medication for seven days. On the seventh day, the animal was sacrificed. Plasma levels of Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), Glutathione (GSH), total antioxidant capacity (TAC), Caspase۳, Malondialdehyde (MDA), Interleukin-۶ (IL-۶), and tumor necrosis factor-alpha (TNF-) were measured in the cardiac blood samples. Vitamin B۱۲ lowers liver enzyme levels in the blood, increases overall antioxidant levels, and compensates for tissue glutathione deficiency while lowering serum elevations. TNF-α and interleukin-۶ levels are also reduced by caspase۳. Acetaminophen-induced hepatic necrosis and inflammatory cell infiltration were both considerably reduced by vitamin B۱۲ supplementation. According to this study, vitamin B۱۲ was found to have a protective effect against acetaminophen-induced hepatotoxicity.