Introduction. Methemoglobinemia is a condition characterized by increased quantities of hemoglobin in which the iron of heme is oxidized to the ferric(Fe3+) form. Methemoglobin is useless as an oxygen carrier and thus causes a varying degree of cyanosis. The condition may arise as a result of a genetic defect in red blood cell metabolism or hemoglobin structure, or it may be acquired following exposure to various axidant drugs or toxins. The most common cause of methemoglobinemia, as in this clinical case, is ingestion of or exposure of skin or mucous membranes to oxidizing agents (such as anesthetics and silver nitrate). Methods. In an experimental animal study, 30 rabbits with the same weight and sex are devided in two groups (A and B).-Vitamine C is administered to group B (200 mg/kg intraperitoneal). One houre after that, laparotomy was done. Then silver nitrate was injected intraperitoneal (1000 mg/kg) in both groups. Blood samples were examined 30 and 60 minutes after injection. Results. Methemoglobin before and after intervention in group A was 0.38±0.13, 1.63±0.02 (30 min) and 2.21 ± 0.4 (60 min) percent respectively. Methemoglobin before and after intervention in group B was 0.39±0.13, 0.82 ± 0.19 (30 min) and 0.41 ± 0.1.7 (60 min) percent, respectively. Methemoglobin concentration was greater in group A in 30th and 60th minute after intervention (P < 0.0l) Discussion. Ascorbic acid penetrate the erythrocyte membrane. Under physiological conditions ascorbic acid induced methemoglobin reduction is far less important than reduction by the NADH dependent methemoglobin reductase system. In methemoglobinemic conditions caused by toxic effects or by congenital methemoglobin reductase deficiency treatment with ascorbic acid is possible. However, critically increased methemoglobin content of the blood higher than 30% makes therapy with methylene blue necessary. So, vitamine C is recommended for methemoglobinemia therapy.