Effects of Amylase and Invertase Regulators Upon Sugar Content, Protein Content, and Enzyme Activity of Immature Sugarcane

Immature sugarcane grown in sand culture was treated with manganese, an in vitro activator of amylase and invertase, and with mercury, an in vitro inhibitor of the same enzymes. Both elements were supplied as foliar sprays and as nutrient-solution supplements. The objective was to determine whether in vivo effects would be equivalent to those observed in the test tube, and to determine the effects of these elements on sugar content. Leaf and meristem tissues wore frozen and lyophilized for sugar and enzyme assay. Mercury solution of 1,000-p.p.m. concentration caused a marked suppression of leaf amylase activity and sucrose content, which persisted 27 days after treatment. The major mercury effect was confined to the leaves. In meristem tissues, sucrose changes as established by control plants were enhanced by mercury and alleviated by manganese. Mercury at 1,000 p.p.m. caused a moderate invertase suppression which disappeared by 27 days after treatment. Plants receiving mercury and manganese as nutrient-solution supplements- experienced major sugar changes in meristem rather than leaves. Low manganese, and both high and low mercury, greatly suppressed sucrose content. Arsenate, which was also being tested, likewise caused marked deterioration of meristem sucrose. Invertase was generally stimulated among plants receiving additives through their roots. Amylase was not affected. Mercury, an extremely efficient invertase inhibitor in the test tube, more than doubled invertase activity in plants receiving 0.05 p.p.m. of mercury in their nutrient solutions. In vivo effects of manganese and mercury did not agree well with expectations based on in vitro observations. Liven in those instances where (he anticipated results were gained, these required far greater concentrations of additive than should have been necessary. Nevertheless, definite influences were exerted upon both amylase and invertase. Discrepancies between in vivo and in vitro results are discussed. It is suggested that these differences are attributable to the positioning of in vivo catalysts in reaction sequences, to the stimulation of protein production by treatment additives, and to the increased production of nonprotein, endogenous enzyme activators and inhibitors