705the present ones which suggest the existence of a photochemical reaction between D N A and bilirubin are somewhat disquieting, particularly when one considers that mutagens and chemical carcinogens derive their biologic activity from the ability to react with DNA. Our results suggest that phototherapy of neonates is a complex process which may generate a number of potentially dangerous genetic side effects. S U M M A R YThe widespread use of phototherapy in the treatment of neonatal jaundice is causing concern because little information is available on its effects on subcellular structure and function. The present study deals with the effects on the macromolecular structure of D N A illuminated in the presence of bilirubin. The results indicate a bilirubin-induced photodegradation of this biopolymer. ExtractAlthough the precise etiologic incitant of the minimal lesion idiopathic nephrotic syndrome of childhood is not known, it is likely that a host mechanism mediates the permeability alterations of the glomerular capillary wall resulting in massive proteinuria. As a first step in examining the possibility that local kinin release may account for the proteinuria in this disorder, two parameters of the plasma kinin-generating system, plasma prekallikrein and kallikrein inhibitor, were assayed during 27 nephrotic episodes in 21 corticosteroid-responsive children. Plasma kallikrein was assayed by means of its esterase activity on a synthetic arginine ester substrate, N-a-tosyl-L-arginine methyl ester (TAMe), after activation of Hageman factor by kaolin. This activity, after subtraction of spontaneous arginine esterase activity (i.e., TAMe esterase activity measured in plasma not exposed to kaolin) is derived from prekallikrein. Plasma prekallikrein activity in 11 normal children was 99.6 + 2.9 pnol TAMe hydrolyzed/ml plasma/hr (mean + SEM). Kallikrein inhibitor was quantified in arbitrary units. Kallikrein inhibitor activity in 11 normal children was 0.94 + 0.04 units.During the overt nephrotic syndrome, before initiation of intensive daily corticosteroid treatment, mean values were: prekallikrein, 58.5 A 7.24 flmol/ml/hr; and kallikrein inhibitor, 0.35 + 0.06 units. After corticosteroid-induced remission occurred, mean values were: plasma prekallikrein, 118.6 + 3.2 pmol/ml/hr; and kallikrein inhibitor, 0.78 + 0.03 pmol/ml/hr. Both parameters were again assayed in 14 of the 21 children after complete cessation of corticosteroid treatment. Plasma prekallikrein was normal, 99.6 * 4.8 flmol/ml/hr; but kallikrein inhibitor was still somewhat depressed, 0.84 + 0.03 units. A subset of 9 patients had marked depression of plasma prekallikrein to levels less than 20 pmol/ml/hr and essentially undetectable inhibitor acGvity. Serum a-2 macroglobulin was elevated in nephrotic patients: mean value during relapse, 862 + 29 mg/100 ml; during corticosteroid-maintaining remission, 615 * 29 mg/100 ml. After cessation of corticosteroids, mean serum level was 481 + 20 mg/100 ml. The proportional reduction of plasma prekallikrein an...