This review describes the historic background of the discovery of vitamin B_<12> that began with the clinical study made by Minot and Murphy who successfully treated patients with pernicious anemia by feeding large quantities of beef liver. It was followed by a series of human experiments conducted by Castle who elaborately demonstrated that hemopoiesis required an exogenous food (extrinsic) factor as well as an endogenous factor that resided in the gastric juice (intrinsic factor). Led by this hypothesis, the extrinsic factor was subsequently identified in the liver as vitamin B_<12> and the intrinsic factor as a glycoprotein produced by the parietal cells of the stomach. Based on these studies and discoveries, pernicious anemia is now an established autoimmune disease with an epitope residing in the membrane of the parietal cell.

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To understand the effects of lipid peroxides on physiological function of small intestine, rat small intestinal mucosa was incubated with 2, 2'-azobis (2-amidinopropane) dihydrochloride (AAPH), a free radical generator in aqueous phase, and changes in the level of lipid peroxidation, protein content, and enzymatic activities of maltase, lactate dehydrogenase (LDH) and mitochondrial dehydrogenase were analyzed. We also examined preventive effects of α-tocopherol and L-ascorbic acid against such changes. Incubation of small intestinal mucosa with AAPH resulted in the increase of thiobarbituric acid reactive substances (TBARS). Similar treatment induced reduction of the maltase activity. Addition of α-tocopherol and L-ascorbic acid prevented the increase of TBARS induced with AAPH, although the inhibitory effect on maltase level did not change unless 500 μg/mg protein of L-ascorbic acid was added. Likewise AAPH lowered the level of LDH and mitochondrial dehydrogenase activities, which was not influenced by α-tocopherol. These results demonstrate that AAPH treatment causes cellular damage, indicating that both lipids and proteins are attacked by free radicals. Further investigation is necessary to clear preventive effects of antioxidative vitamins against change in proteins and cellular injury caused with AAPH in small intestine.

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