Since the paper by Somers & Shive (1942), on the iron-manganese relation in plant metabolism, numerous workers have carried out investigations directed to test the validity of their hypothesis which suggests that the physiologically active iron is in the ferrous state and that manganese regulates the concentration of ferrous iron in the cell. Arnon (I1943), in his consideration of this hypothesis, points out that it is doubtful whether plants can utilize only ferrous iron, since the iron porphyrin enzyme systems involve the reversible reaction ferric to ferrous. Since manganous manganese is supplied to plants, on the basis of Somers's and Shive's hypothesis, the manganous ion must be oxidized to the manganic ion which can then oxidize the ferrous iron; a system whereby manganese can be oxidized in higher plants has been demonstrated by Kenten & Mann (I949). Nevertheless, as pointed out by Hewitt (I948 a), hypotheses based on oxidation-reduction potentials of simple ions are probably inadequate to explain the effect of certain metals (e.g. copper) in inducing iron deficiency, and much more information is required regarding the nature of the complex metalo-compounds formed. With regard to the heavy-metal induced iron chlorosis, it has been suggested by Sideris & Young (1949) that manganese instead of iron may react with porphyrin compounds thereby inactivating them for subsequent conversion to chlorophyll; Hewitt (I948 b) envisages manganese and other heavy metals with similar ionic radii, valency and electronic configuration competing with iron and blocking a reaction leading to chlorophyll formation. Such reactions with heavy metals may intensify the chlorotic state, but reactions in iron metabolism result in the formation of at least two iron fractions. Oserkowsky (I933), Jacobsen (I945) and Bennett (1946) have all postulated the existence of 'active' and 'inactive' forms of iron, the active form being a protein in close association with or in the chloroplasts. The results of the experiments reported here support, in general, the existence of active and inactive forms of iron. Somers & Shive (1942) suggested that manganese deficiency was iron toxicity and iron deficiency was manganese toxicity. Several workers (Morris & Pierre I947; Berger & Gerloff, 1947; Hewitt, 1948 a) observed the symptoms of manganese toxicity to be quite distinct from those of iron deficiency, but mild forms of the toxicity are in my experience identical with iron deficiency. Morris & Pierre (I947) showed that manganese toxicity could be prevented by increasing the iron supply; this was due to antagonism whereby the amount of manganese absorbed was reduced by 50 %Wallace & Hewitt (1946) state 'although manganese has been clearly shown in solution culture to be antagonistic to iron it appears unlikely to be an important factor in lime-induced chlorosis'; in the experiments described in this paper the effect of manganese on the absorption of iron is