Vol. 94, No. 2 April, 1948 THE BIOLOGICAL BULLETIN PUBLISHED BY THE MARINE BIOLOGICAL LABORATORY RETARDATION OF CELL DIVISION BY VITAMIN C IN PHYSIOLOGICAL CONCENTRATIONS HERBERT SHAPIRO* From the Laboratory of Physical Biology, National Institute of Health, Bethcsda, Maryland, and the Marine Biological Laboratory, Woods Hole, Mass. 1. ON THE MECHANISM OF THE ACTION OF ASCORBIC ACID IN THE BODY Although numerous studies have been carried out on the gross and microscopic changes occurring in tissues in vitamin C deficiency, the mechanisms by which the effects are produced are still largely unresolved. A survey of the pathological changes leads to the conclusion that the primary effect of ascorbic acid deficiency is an abnormality in the intercellular material, or perhaps at the cell surface, leading to changes in the bones and small blood vessels. In cases of this vitamin deficiency, formation of cartilage and bone is stopped, and the junction of epiphysial cartilage and bone is weakened. The widespread oc-currence of hemorrhages points to the failure of the cells in the vessel walls to ad-here normally and retain their functions as closed tubes, impervious to erythrocytes. This is due to failure in the formation and maintenance of intercellular materials and consequent weakness of the tissue (Wolbach and Bessey, 1942). The phe-nomena are of considerable interest to the cellular physiologist for they point clearly to some relation between cell structure and pathology, arising from a biochemical deficiency. Some of these questions of cellular action have been covered in a re-view by Reid (1943). It appeared to be of some value to investigate the influence of 1-ascorbic acid on cell division, because of the likelihood of some action on the cell surface, which might alter conditions there so as to produce an effect on cell division which can be measured quantitatively by known methods (Shapiro, 1941). Results to date indicate that ascorbic acid does not play a major role in tissue respiration since vitamin C depleted tissues show little reduction of oxygen consumption, and but a small increase when the vitamin is added (Stotz and Harrer, 1937). Stark, Gordon and Christensen state (in Elvehjem and Wilson, 1939), "it must be recog-nized that there has been assigned to ascorbic acid no respiratory function in animal physiology." This does not exclude the possibility that vitamin C might still play a minor role in cell oxidations, at the same time that it -determines the form of the histological picture. * Special Research Fellow, Laboratory of Physical Biology, National Institute of Health, Bethesda, Maryland. 79
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