Bis(2-ethylhexyl) phthalate (DEHP) is a frequently used plasticizer with pronounced hepatotoxic and nephrotoxic potentials. This study evaluated the protective effect of ubiquinone (Coenzyme Q, Q10) against DEHP-induced hepatorenal injury in juvenile rats. Forty male Sprague-Dawley rats (3 weeks old) were allocated into four groups: control, Q10 (10 mg/kg b.wt), DEHP (500 mg/kg b.wt), and DEHP+Q10 in a 35-day oral-dosing study. DEHP considerably raised liver enzymes (GGT, ALT, ALP, and AST), bilirubin, creatinine, urea, uric acid, and lipid fractions (TG, TC, VLDL-C, and LDL-C), while reducing total protein, albumin, and HDL-C. Hepatic and renal antioxidant defenses (GSH, SOD, and CAT) were markedly repressed, accompanied by a sharp rise in MDA, and apoptotic and pro-inflammatory mediators (caspase-3, TNF-α, and IL-6) were significantly upregulated. Histologically, DEHP induced severe hepatocellular degeneration, vascular congestion, portal inflammation, glomerular atrophy, and tubular necrosis. Immunohistochemically, DEHP markedly suppressed Nrf2 and PPAR-γ expression while strongly inducing CD4 immunopositivity in both liver and kidney tissues; Q10 co-treatment significantly reversed these alterations. Q10 supplementation markedly ameliorated these biochemical and structural alterations, restoring the redox balance, reducing lipid peroxidation, improving markers of renal and hepatic function, and alleviating histopathological lesions. These findings highlight the hepatorenal protective potential of Q10 against DEHP-induced toxicity through antioxidant, anti-apoptotic, and anti-inflammatory mechanisms.