Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04179 (MnSOD)
2,777 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

5-Aminolevulinic acid (ALA), a heme precursor that accumulates in acute intermittent porphyria patients and lead-exposed individuals, has previously been shown to autoxidize with generation of reactive oxygen species and to cause in vitro oxidative damage to rat liver mitochondria. We now demonstrate that chronically ALA-treated rats (40 mg/kg body wt every 2 days for 15 days) exhibit decreased mitochondrial enzymatic activities (superoxide dismutase, citrate synthase) in liver and soleus (type I, red) and gastrocnemius (type IIb, white) muscle fibers. Previous adaptation of rats to endurance exercise, indicated by augmented (cytosolic) CuZn-superoxide dismutase (SOD) and (mitochondrial) Mn-SOD activities in several organs, does not protect the animals against liver and soleus mitochondrial damage promoted by intraperitoneal injections of ALA. This is suggested by loss of citrate synthase and Mn-SOD activities and elevation of serum lactate levels, concomitant to decreased glycogen content in soleus and the red portion of gastrocnemius (type IIa) fibers of both sedentary and swimming-trained ALA-treated rats. In parallel, the type IIb gastrocnemius fibers, which are known to obtain energy mainly by glycolysis, do not undergo these biochemical changes. Consistently, ALA-treated rats under swimming training reach fatigue significantly earlier than the control group. These results indicate that ALA may be an important prooxidant in vivo.
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PMID:5-aminolevulinic acid-induced alterations of oxidative metabolism in sedentary and exercise-trained rats. 153 18

Seventy male factory workers were studied. The lead concentrations in their blood (Pb-B) were 16.55 +/- 11.53 micrograms/100 ml (range 1.5 to 50.2 micrograms/100 ml). The subjects were divided into three groups according to Pb-B (in microgram/100 ml): group A, Pb-B < or = 10 (n = 22); group B, 10 < Pb-B < or = 20 (n = 30); group C, Pb-B > 20 (n = 18). The mean +/- S.D. in each group was 5.57 +/- 2.53, 15.02 +/- 2.75, and 32.52 +/- 9.49 micrograms/100 ml, respectively. Pb in plasma was 0.011 +/- 0.010, 0.017 +/- 0.033, and 0.021 +/- 0.021 microgram/liter, and Pb in the RBC was 0.281 +/- 0.246, 0.701 +/- 0.325, and 1.626 +/- 0.861 micrograms/g Hb, respectively. In addition to Pb concentration, the concentrations of 34 elements in the plasma or in the RBC were determined. Se concentrations in RBC in each group were 0.618 +/- 0.139, 0.670 +/- 0.207, and 0.728 +/- 0.200 microgram/g Hb, and the mean values were significantly different between groups A and C (p < 0.05). For Se concentration in plasma, the mean +/- S.D. in each group was 0.132 +/- 0.035, 0.130 +/- 0.031, and 0.126 +/- 0.021 microgram/ml, respectively, and there was no significant difference between groups. On the other hand, when the activities of total SOD, Mn-SOD, Cu, Zn-SOD, and catalase in the plasma and the activities of GSH-Px both in the plasma and in the RBC were assayed, some differences were found. The activities in GSH-Px in RBC were 17.19 +/- 5.03, 17.59 +/- 3.95, and 15.25 +/- 3.18 mumol/g Hb/min, and those in plasma were 0.069 +/- 0.032, 0.081 +/- 0.023, and 0.080 +/- 0.028 mumol/ml/min. In group C, GSH-Px activity was lower in the RBC and higher in the plasma than those in group A, and it was observed that the Se concentration was higher in RBC, and that there was no remarkable change in the plasma. Catalase activity in group C was 3.58 +/- 0.81 mgH2O2/ml/30 min, which was significantly higher than that in group A (2.81 +/- 0.90 mgH2O2/ml/30 min). Further investigation is necessary in order to explain the above results. The regular indices used for evaluating lead exposure, showed significant correlations with Pb-B: r = -0.786 vs delta-Aminolevulinic acid (ALA) dehydratase activity in blood, r = 0.927 vs. inhibition rate, and r = 0.339 vs. ALA in urine.
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PMID:Indices of lead-exposure in blood and urine of lead-exposed workers and concentrations of major and trace elements and activities of SOD, GSH-Px and catalase in their blood. 884 89