Purine salvage enzymes (ADA, PNP, HGPRT) are important in lymphocyte differentiation and proliferation. But the effect of antineoplastic agents on purine metabolism is poorly understood. We studied in vivo effects of several antineoplastic agents on these enzyme activities in L1210 mouse leukemic cells. L1210 cells were injected into peritoneal space of BDF/1mouse, followed by antineoplastic agent at 6-7 days later. After 6 hrs of exposure to MTX, ADA activity and PNP activity were slightly inhibited. On the contrary, HGPRT activity was activated remarkably. Daunorubicin inhibited PNP activity slightly but it had no effect on ADA activity and HGPRT activity. Coformycin inhibited ADA activity severely but it had no effect on PNP and HGPRT activity. These observation suggest that the block of de novo purine synthesis may result in reduced activity of purine interconversion enzyme and activated purine salvage synthesis. But further study is needed.
Hyperuricemia occurs frequently in essential hypertension. We analysed influences of hypertension and ageing on serum uric acid and serum creatinine by epidemiological study of 805 women and 528 men over 40 years old in Hakushucho, Yamanashi Prefecture. Normotensive subjects (n=635), borderline hypertension (n=330) and established hypertension (n=368) were classified by WHO criteria of hypertension. Serum uric acid increased slightly along with ageing in all groups (but insignificantly). On the contrary, a significant correlation was demonstrated between serum uric acid and ageing in normotensive subjects and borderline hypertension. But no significant correlation was found in established hypertension. Serum uric acid concentration in established hypertension was the highest of all groups and its concentration in borderline hypertension was higher than those of normotensive subjects. Positive correlation was observed between serum uric acid and serum creatinine in all groups. These data suggest that hyperuricemia in hypertension is associated with the height of the blood pressure and renal involvement.
The author examined the serum uric acid in diabetic coma and concluded in the following: 1. Hyperuricemia was present in all patients with hyperosmolar non-ketotic diabetic coma (HNC), diabetic ketoacidosis (KA) and lactic acidosis (LA). 2. The cause of hyperuricemia is ketosis in KA and lactate in LA. The reduction of body fluid and urine flow and renal damage may explain the hyperuricemia in HNC. 3. After 4-5 days treatment, the serum uric acid returned to normal range. 4. The degree of increase of the serum uric acid is larger in KA and LA than in HNC.
The author measured the serum uric acid in 150 diabetic patients and found 8 cases with hypouricemia (below 2.5mg/dl). Eight diabetic patients with hypouricemia were summarized in the following. 1. There were less frequent with obesity, Hypertension, hypertriglyceridemia and over drink. 2. The complication of retinopathy and nephropathy were rare. 3. The state of blood glucose control was poor in all cases. 4. The increased CuA and CuA/Ccr ratio were found in all of 6 cases measured.
The auther measured the serum uric acid in 6 patients with acute hepatic failure and gained the results in the followings. 1. Hypouricemia below 2.0 mg/100ml was present in 4 of 6cases. 2. Urinary uric acid excretion was increased. 3. There was inverse relation between total bilirubin and serum uric acid. 4. The causes of hypouricemia in acute hepatic failure might be mainly decreased urate synthesis and partially increased renal excretion of uric acid.