The effect of arsenate on cells of a marine cyanobacterium, Phormidiurn sp. preliminarily starved for phosphate for a week was studied. Cells were harvested and cultured in artificial seawater containing various concentrations of arsenate and phosphate. Arsenate at concentrations above 30 mg As dmP3 inhibited biosynthesis in the cells and consequently, growth when incubated without phosphate in the medium. On the contrary, phosphate at 50 pmol dm-3 was sufficient for apparently complete cancellation of the inhibitory. effects of arsenate at concentrations up to 150 mg As dm-3. Study of the carbohydrate metabolism revealed an intense inhibition by arsenate on turnover of carbohydrate to other cell components in the phosphate-depleted cells. This resulted in a color change of the cells from blue-green to yellowish. The synthesis of carbohydrate itself was also inhibited by arsenate. Arsenate incorporation into cells was clearly inhibited by phosphate in the medium, suggesting that arsenate competes with phosphate for entry into cells. In addition, arsenate incorporated in cells could not inhibit the incorporation of phosphate and subsequent growth of cells on phosphate. These observations indicate that arsenate can act as a poisonous substitute for phosphate in the cells but, once incorporated into the phosphate-replete cells, it no longer has an inhibitory effect. The inhibitory effects of arsenate seem to be mainly related to ATP synthesis in the photosynthetic system.

The mechanism of arsenate incorporation in the cells of a unicellular marine cyanobacterium, Synechococcus sp., was investigated. A lag period in arsenate incorporation, probably caused by an inhibitory effect of phosphate absorbed on the cell surface, was observed. Although arsenate incorporation into the cells of cyanobacterium was several times faster than that of phosphate, it was readily inhibited by addition of phosphate, also suggesting inhibition caused by phosphate. The Michaelis-Menten type of equation was employed for the simulation of incorporation, and a nonlinear fitting was applied for the estimation of the kinetic parameters in the equation. Analysis based on the assumption that arsenate is incorporated via the phosphate transport system in cells suggested that arsenate competes with phosphate for entry into cells and each species acts as a competitive inhibitor to each other. The affinity of arsenate with the transport system was much less than that of phosphate, but it was not low enough for elucidation of an almost complete inhibition of arsenate incorporation by phosphate, and another mechanism to block the approach of arsenate to the transport system was deduced to exist. The inhibitory effect of phosphate on arsenate incorporation seemed responsible for alleviation of the toxicity of arsenate in the cells.