The opioid painkiller tramadol (TML) is frequently used to treat moderate to severe pain. On the other side, TML is frequently misused in many nations due to its accessibility and low price. High doses or prolonged administration of TML are linked to hepatic and renal damage. There is currently no known precise mechanism for how TML damages the liver and kidneys. The goal of the current investigation was to assess the potential contribution of oxidative stress dysfunction to the etiology of renal and hepatic injury brought on by TML. For this purpose, male adult rats were treated with TML (15 and 30 mg/kg/day oral administration) 30 days in a row. A significant decrease in liver and kidney tissue SOD, CAT, NO, and MAD was detected in TML groups, while, hepatic and Renal histopathological alterations included inflammation, necrosis, hemorrhage, and congestion, in TML-treated animals, generally, the complementary results of the histological study, by evaluating the degree of histopathological changes, the distribution of lesions by scores (Sc) and an important factor (Fi), and the injury severity index in both kidney and liver tissue, revealed the severity of the pathological changes in the highest dose group compared with the rest of the groups. On the other hand, TML (30 mg/kg/day) caused more dysfunction in the studied biomarkers compared to the other groups. Prolonged tramadol use carries a risk of greater hepatic and renal damage. As such, tramadol’s harmful effects must be taken into account during ongoing treatment.
Keywords | Tramadol, Functional, Histopathology, Oxidative stress, Antioxidants, Biochemical indices, Liver, Kidney, Rat