Restorative effect of Sb and CSbnp were indicated by the improved antioxidant status. However, compared to the Sb-treated group, CSbnp-treated rats demonstrated much closer SOD, catalase and GSH levels to those of the control group. Silymarin was reported to have protective effect on diabetes induced oxidative damages in the pancreas, kidney and liver. The antioxidant effect of silymarin components is mainly due to its antiradical and reactive oxygen species scavenging capacities. Additionally polyphenolic silymarin compounds may play an important role in Alisol-G stabilizing lipid peroxidation due to their intrinsic reducing capacity. Pancreatic tissue histoarchitecture of CSbnpT group recorded a marked improvement in the structural integrity of the islets of Langerhans when compared to the observations in group D. Islet histoarchitecture, the number of islet cells and peripheral islet infiltration of lymphocytes appeared to be considerably improved. On the other hand, Sb treated group exhibited better histoarchitecture of islet cells with partial recovery in comparison to diabetic group. Liver sections of non-diabetic control animals exhibited regular hepatic architecture, prominent centrilobular vein,Alisol-F sinusoidal spaces and prominent nucleus. In contrast, sections of the diabetic rat liver showed accumulation of fat droplets with distorted morphology of centrilobular vein, hepatocytes, and occurrence of sinusoidal dilatation. Treatment with engineered nanoparticles stimulated significant revival of hepatic cytoarchitecture with reduction of fat droplets as well as sinusoidal abnormality. The revival effect appeared to be better compared to that of Sb-administered animals. Streptozotocin is a nitrosourea analog which is known to accumulate selectively in pancreatic beta cells via the low-affinity glucose transporter-2 in the plasma membrane. Selective toxicity of this agent causes DNA alkylation, protein glycosylation and depletion of ATP leading to beta cell damages. Insulin biosynthesis, glucose-induced insulin secretion and glucose metabolism get affected as a result of impaired beta cell functions. Hyperglycemic conditions in diabetes leads to free radicals generation and induces oxidative stress by activating mitochondrial NADPH oxidase.