A significant minority of the vitamin C in plants is located in the apoplast. We discuss recent progress towards mapping the pathway by which apoplastic L-ascorbate is converted to oxalate plus L-threonate. At least two novel compounds have been detected as apoplastic intermediates in the pathway: namely, 4-O-oxalyl-L-threonate and cyclic oxalyl di-ester(s) of Lthreonate. In addition, evidence is presented for a dehydroascorbate oxidase activity and two novel oxalyl-esterase activities involved in the pathway. The operation of the pathway may augment the proposed role of ascorbate as a pro-oxidant since several steps in the pathway potentially generate H 2 O 2 . We argue that, whether acting as a pro-oxidant or in its better-known capacity as an anti-oxidant, apoplastic ascorbate may loosen the cell wall and hence promote cell expansion and/or fruit softening.Abbreviations: A, dehydro-L-ascorbate; AH 2 , L-ascorbate; AO, L-ascorbate oxidase; D, cyclic oxalyl di-ester(s) of Lthreonate; F, 4-O-oxalyl-L-threonate.

We have examined the filterability of sickle erythrocytes, using an initial-flow-rate method, to determine whether sufficient hemoglobin S polymer forms at arterial oxygen saturation to adversely affect erythrocyte deformability. The amount of intracellular polymer was calculated as a function of oxygen saturation to estimate the polymerization tendency for each of eight patients with sickle cell anemia (SCA). Progressive reduction of oxygen tension within the arterial range caused a sudden loss of filterability of SCA erythrocytes through 5-,nmdiam pores at a critical P02 between 110 and 190 mmHg. This loss of filterability occurred at a higher P02 than did morphological sickling, and the critical Po2 correlated significantly (r = 0.844-0.881, P < 0.01) with the polymerization tendency for each patient. Study of density-gradient fractionated cells from four SCA patients indicated that the critical P02 of dense cells was reached when only a small amount of polymer had formed, indicating the influence of this subpopulation on the results obtained for unfractionated cells. Impairment of erythrocyte filterability at high oxygen saturation (> 90%) suggests that small changes in oxygen saturation within the arterial circulation cause Theological impairment of sickle cells.