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PubMed2002

Effect of microsomal enzyme inducers on the biliary excretion of triiodothyronine (T(3)) and its metabolites.

It has been postulated that inducers of UDP-glucuronosyltransferase (UGT) decrease circulating thyroid hormone concentrations by increasing their biliary excretion. The inducers pregnenolone-16 alpha-carbonitrile (PCN), 3-methylcholanthrene (3MC), and Aroclor 1254 (PCB) are each effective at reducing serum thyroxine concentrations. However, only PCN treatment produces a marked increase in serum levels of thyroid-stimulating hormone (TSH), whereas 3MC and PCB cause little to no increase in TSH. Excessive TSH elevation is considered the primary stimulus for thyroid tumor development in rats, yet the mechanism by which enzyme induction leads to TSH elevation is not fully understood. Whereas PCN, 3MC, and PCB all increase microsomal UGT activity toward T(4), only PCN causes an increase in T(3)-UGT activity in vitro. The purpose of this study was to determine whether PCN, which increases serum TSH, causes an increase in the glucuronidation and biliary excretion of T(3) in vivo. Male rats were fed control diet or diet containing PCN (1000 ppm), 3MC (250 ppm), or PCB (100 ppm) for 7 days. Animals were then given [(125)I]-T(3), i.v., and bile was collected for 2 h. Radiolabeled metabolites in bile were analyzed by reverse-phase HPLC with gamma-detection. The biliary excretion of total radioactivity was increased up to 75% by PCN, but not by 3MC or PCB. Of the T(3) excreted into bile, approximately 75% was recovered as T(3)-glucuronide, with remaining amounts represented as T(3)-sulfate, T(2)-sulfate, T(3), and T(2). Biliary excretion of T(3)-glucuronide was increased up to 66% by PCN, while neither 3MC nor PCB altered T(3)-glucuronide excretion. These findings indicate that PCN increases the glucuronidation and biliary excretion of T(3) in vivo, and suggest that enhanced elimination of T(3) may be the mechanism responsible for the increases in serum TSH caused by PCN.

Animals↗
PubMed2002

Increase in bile flow and biliary excretion of glutathione-derived sulfhydryls in rats by drug-metabolizing enzyme inducers is mediated by multidrug resistance protein 2.

Glutathione (GSH) is an important cellular constituent for normal liver homeostasis. Certain drug-metabolizing enzyme inducers (i.e., phenobarbital [PB] and pregnenolone-16alpha-carbonitrile [PCN]) increase biliary excretion of GSH-derived sulfhydryls (SH) as well as bile flow, whereas other drug-metabolizing enzyme inducers (i.e., 3-methylcholanthrene [3MC] and benzo(a)pyrene [BaP]), do not. The purpose of the study was to determine whether rat multidrug resistance protein 2 (Mrp2) is the inducible transporter responsible for increasing biliary SH excretion and bile flow. Sprague-Dawley (SD) rats were injected ip daily for 4 days with PB, PCN, 3MC, BaP, or vehicle; Mrp2-null Eisai hyperbilirubinemic (EHBR) rats were injected ip daily for 4 days with PCN or vehicle. Although no drug-metabolizing enzyme inducer altered hepatic GSH in SD rats, PB and PCN significantly increased the rate of biliary SH excretion and bile flow. Neither 3MC nor BaP affected the biliary SH excretion rate or bile flow. In control EHBR rats, despite elevated hepatic GSH, the rate of biliary SH excretion was almost completely eliminated and bile flow was dramatically reduced compared with SD rats. Furthermore, PCN treatment did not affect bile flow or the biliary SH excretion rate in EHBR rats. PB and PCN also increased Mrp2 protein levels, but 3MC and BaP did not. None of the drug-metabolizing enzyme inducers tested significantly increased Mrp2 mRNA levels. PCN increased Mrp2 protein, but not Mrp2 mRNA, in a time-dependent manner. In conclusion, Mrp2 is the inducible efflux transporter responsible for increased biliary SH excretion and bile flow after administration of some drug-metabolizing enzyme inducers.

ATP-Binding Cassette Transporters↗
PubMed1981

Effect of bile induced pancreatitis on tobramycin excretion in pancreatic fluid.

The objective of this study has been to lay the groundwork for a re-evaluation of the place of antibiotics in acute pancreatitis. This section has been devoted to determining if antibiotics excreted by the normal pancreas are excreted similarly in acute pancreatitis. Ten mongrel dogs were studied, each acting as its own control. Day 1: Operation--construction of pancreatic fistula. Day 2: Study of antibiotic excretion. Day 14: Operation--induction of acute focal pancreatitis. Day 15: Study of antibiotic excretion. Antibiotic concentrations in pancreatic fluid were studied by injecting tobramycin intravenously (5 mg/kg). Serum levels and excretion of the drug in the pancreatic secretion were then monitored over the next six hours. Results showed excretion of tobramycin reached bactericidal concentrations in pancreatic fluid from the normal and inflamed pancreas, with no significant differences (p = 0.2) between the excretion rates. The place of antibiotics in acute pancreatitis is discussed. Based on usual pathogens isolated in pancreatic abscesses, and their usual sensitivity patterns, tobramycin with Cephamandole are the antibiotics of choice in acute pancreatitis, and a clinical trial is indicated to evaluate their place in reducing complications and deaths in the disease.

Acute Disease↗
PubMed1985

Whole-body protein breakdown and 3-methylhistidine excretion during brief fasting, starvation, and intravenous repletion in man.

Simultaneous whole-body protein breakdown (using 15N-glycine) and urinary 3-methylhistidine (3MH) excretion rates were determined in six hospitalized normal volunteers after 10 days of starvation and a subsequent 10-day period of total parental nutrition (TPN). These data were contrasted to whole-body protein breakdown and urinary 3MH excretion in ten depleted (14.8% body weight loss) patients with benign intraabdominal disease studied in the basal (48 hours without nutrient intake) and intravenously refed states. The rates of whole-body protein breakdown were significantly reduced from basal (brief fasting or starvation) conditions in both normal volunteers (p less than 0.01) and depleted patients (p less than 0.01) during TPN. The rate of protein catabolism normalized for creatinine excretion in patients was higher than that observed in normal subjects during both basal (p less than 0.05) and intravenous feeding conditions. Daily urinary 3MH excretion was reduced during intravenous feeding in both starved normal volunteer (235 +/- 13 mumol/d to 197 +/- 9 mumol/d p less than 0.05) and in depleted patients (209 +/- 31 mumol/d to 140 +/- 35 mumol/d), and an apparent linear relationship between protein breakdown and urinary 3MH, normalized for creatinine excretion, was obtained in both volunteer and patient (r = 0.85) populations during fasting-refeeding. However, separate regression analysis of the protein breakdown and 3MH responses of both volunteer and patient groups under conditions of fasting, starvation, and refeeding revealed significant differences between volunteer and patient populations during intravenous refeeding (p less than 0.01). Further analysis of 3MH excretion in relationship to nitrogen balance during refeeding suggests a complex relationship between urinary 3MH excretion and whole-body protein metabolism that may be partly related to the degree of antecedent malnutrition.

Adult↗
PubMed2001

Urinary excretion of thioTEPA and its metabolites in patients treated with high-dose cyclophosphamide, thioTEPA and carboplatin.

The urinary excretion of N,N',N"-triethylenethiophosphoramide (thioTEPA), and its metabolites N,N',N"-triethylenephosphoramide (TEPA), N,N'-diethylene,N"-2-chloroethylphosphoramide (monochloroTEPA) and thioTEPA--mercapturate was determined in patients receiving thioTEPA as part of a high-dose combination chemotherapy regimen with cyclophosphamide and carboplatin. The thioTEPA dose was 40 or 60 mg/m(2) in short infusions, twice daily, during 4 days. Urine samples were collected after each voiding on each day of drug administration until 24--48 h after the last thioTEPA infusion. ThioTEPA, TEPA and monochloroTEPA concentrations were determined with gas chromatography and thioTEPA--mercapturate with liquid chromatography--mass spectrometry with direct sample injection. ThioTEPA was present in urine 30 min after infusion and was still excreted 18 h after the last infusion. All metabolites were detected in urine 1 h after infusion. Patients with a creatinine clearance above 140 ml/minl showed higher excretion of TEPA than patients with a creatinine clearance below 140 ml/min (12.8 versus 4.9%, p=0.01). The excretion of monochloroTEPA relative to the excreted amount of TEPA increased at lower pH values of the urine. The excretion of thioTEPA--mercapturate relative to the dose was higher in patients treated with 60 mg/m(2). Excretion of thioTEPA and monochloroTEPA both accounted for only 0.5% of the dose, while TEPA and thioTEPA--mercapturate both accounted for 11.1%.

Acetylcysteine↗
PubMedDate not supplied

The biliary and urinary excretion and the choleretic effect of ioglycamide in dogs.

The biliary and urinary excretion and the choleretic effect of ioglycamide were studied in unanesthetized bile fistula dogs using stepwise increasing infusion rates to obtain multiple steady states. The results are compared with data from previously reported experiments in the same animals using iodoxamate and iodipamide. The rate of biliary excretion and the choleretic effect of ioglycamide are similar to those of iodipamide and iodoxamate. Like iodipamide and iodoxamate, the relation between infusion rate or plasma concentration and biliary excretion or concentration of ioglycamide are hyperbolic and can be fitted to saturation kinetics. Quantitatively, the excretion of ioglycamide and iodipamide are virtually identical. However, for any equimolar infusion rate or plasma concentration, more iodoxamate than ioglycamide is excreted in the bile. Despite the greater biliary excretion of iodoxamate, the maximum biliary concentration of ioglycamide, iodipamide, and iodoxamate is the same at low basal bile flow because the choleretic effects of the three compounds are equal. The data suggest that, theoretically, with any equimolar dose ioglycamide will be identical to iodipamide as a contrast material for intravenous cholangiography, but that iodoxamate may be superior to ioglycamide because more iodoxamate is excreted in the bile. This advantage of iodoxamate might become apparent clinically in patients with high basal bile flow or if smaller doses of the contrast material are used. However, at the presently recommended doses of the two compounds, it is unlikely that the use of ioglycamide for intravenous cholangiography will be any different than iodoxamate.

Animals↗
PubMed1986

A study of 48-hour faecal and urinary electrolyte excretion in normotensive black and white South African males.

Previous studies have shown that 24-h urinary sodium (Na) excretion is similar in blacks and in whites. However, a significantly lower potassium (K) excretion by blacks, with a consequent rise in the Na:K excretion ratio, has been observed. Faecal electrolyte excretion has not been measured. Ten normotensive blacks and 11 normotensive whites on a free diet were studied. Simultaneous 48-h urine and faecal collections were made. The results of the urinary measurements were in accordance with those of previous studies, in that 24-h urinary K excretion by blacks (38.2 +/- 12.4 mmol) was significantly lower than that of whites (78.3 +/- 16.6 mmol). As a result, there was a significantly higher urinary Na:K ratio in the black group. The mean 24-h faecal K excretion of the black group (15 +/- 7.3 mmol) was not significantly lower, even when corrected for weight, than that of the white group (20.8 +/- 10.8 mmol). It is concluded that the low urinary K excretion of South African urban blacks, compared with whites, is a reflection of a lower dietary K intake.

Adult↗
PubMed1992

Is atrial natriuretic peptide-guanosine 3',5' cyclic monophosphate coupling a determinant of urinary sodium excretion in essential hypertension?

OBJECTIVES: (1) To compare urinary guanosine 3',5' cyclic monophosphate (cyclic GMP) excretion between normotensive subjects and essential hypertensive patients; (2) to determine the influence of changes in sodium intake on urinary cyclic GMP excretion in response to the neutral endopeptidase inhibitor candoxatril in essential hypertensives. DESIGN: (1) Twenty-five normotensive subjects and 25 patients with established essential hypertension not on treatment; (2) Single oral dose of candoxatril in eight patients with essential hypertension after equilibration on a low- or high-sodium diet in a placebo-controlled, double-blind, randomized, crossover study. METHODS: Blood pressure was measured by ultrasound sphygmomanometry. Atrial natriuretic peptide (ANP) and urinary cyclic GMP were measured by radioimmunoassay. Group comparisons were made using unpaired t-tests and two-way analysis of variance. RESULTS: Plasma ANP was significantly raised in patients with essential hypertension compared with the normotensive group, but there was no difference in urinary cyclic GMP excretion. Plasma ANP increased significantly on the high- compared with low-sodium diet. After candoxatril, there were significant diet-related increases in plasma ANP and urinary sodium excretion up to 6 h after drug administration. There were similar increases in urinary cyclic GMP excretion on both diets, but there were no consistent differences in this excretion between the low- and high-sodium diets. CONCLUSIONS: These observations not only point to the importance of ANP-cyclic GMP coupling as a determinant of the natriuretic response to endopeptidase inhibition, but also suggest that the excretion of urinary cyclic GMP can be influenced by other factors in addition to circulating ANP.

Atrial Natriuretic Factor↗
PubMed1993

Effect of dietary salt restriction on urinary serotonin and 5-hydroxyindoleacetic acid excretion in man.

OBJECTIVE: To determine the effect of dietary salt restriction on urinary excretion of serotonin and its principal metabolite 5-hydroxyindoleacetic acid (5-HIAA) in man. DESIGN: We studied 16 healthy male volunteers (age range 20-28 years) who ate a standard diet containing 20 mmol/day NaCl, to which either 220 mmol/day NaCl or placebo was added as a supplement for 1 week each, according to a randomized, single-blind crossover design. METHODS: Urinary excretion of serotonin, 5-HIAA, noradrenaline and vanillylmandelic acid (VMA) were measured during the low- and high-salt periods using reverse-phase high-performance liquid chromatography. RESULTS: During the low-salt diet, 24-h urinary excretion of serotonin increased by 42%, accompanied by a 52% rise in the excretion of 5-HIAA. Salt restriction also increased noradrenaline excretion by 77% and VMA excretion by 40%. Regression analysis revealed a strong positive relationship between the excretion of serotonin and of noradrenaline (r = 0.84, P < 0.001) and between that of 5-HIAA and of VMA (r = 0.74, P < 0.001). CONCLUSIONS: Salt restriction stimulates the serotonergic system in man. Stimulation of this system, in conjunction with the sympathetic nervous system, may contribute to renal sodium conservation during dietary salt restriction in man.

Adult↗
PubMed1986

Protein quantity and quality in term and preterm infants: effects on urine creatinine and expression of amino acid excretion data.

The effect of dietary protein quantity and quality on the excretion of creatinine in preterm and term neonatal infants has been investigated. Whey protein predominant formulas result in increased creatinine excretion as compared with either casein protein predominant formulas or with pooled human milk in preterm infants (p less than 0.001 by ANOVA). The volume of human milk (170 versus 185 versus 200 ml/kg/day) appears to have little effect in these infants. In term infants, few differences among the feeding groups were observed, although creatinine excretion did increase with time. The pattern of creatinine excretion among feeding groups was similar regardless of whether or not the data were expressed in milligrams per deciliter or in milligrams per 24 hours. Small correlations of creatinine excretion with birth weight were observed, but these appeared to vary, depending on the type of feeding. These diet-induced differences in creatinine excretion indicate the need for caution in expressing other urinary metabolites, such as amino acids, relative to creatinine excretion.

Amino Acids↗
PubMed1989

Creatinine excretion after renal transplantation.

For alterations in serum creatinine to reflect changes in GFR, urine creatinine excretion must remain constant. Although serum creatinine is often used to monitor chronic changes in allograft GFR, creatinine excretion has not been systematically investigated in renal transplant recipients. In the present study, creatinine excretion was examined in 100 patients who survived at least 12 months with functioning renal allografts. Overall, there was a progressive decline in creatinine excretion from 1420 +/- 410 mg/24 hr at 3 months to 1240 +/- 394 mg/24 hr at last follow-up, 89 +/- 35 months after transplantation (mean +/- SD). The decline in creatinine excretion was greatest in those who subsequently returned to dialysis (-27.4 +/- 20.2%, P less than .05) compared with those who died (-6.9 +/- 24.1%), or survived with functioning allografts (-3.7 +/- 18.1%). Multivariate analysis demonstrated that age, sex, body weight, obesity, diabetes, and cumulative average daily corticosteroid dose (factors that affect muscle mass) all influenced creatinine excretion. However, early post-transplant clinical parameters failed to predict patients who subsequently had declines in creatinine excretion. Thus, it was not possible to predict patients in whom chronic changes in allograft function would be underestimated by changes in serum creatinine. Although clinically relevant functional alterations can be detected by changes in serum creatinine, additional measures of GFR should be used to complement the serum creatinine and monitor chronic changes in allograft function after renal transplantation.

Age Factors↗
PubMed1991

The relationship of urinary thromboxane excretion to cyclosporine nephrotoxicity.

Alterations in renal prostaglandin production have recently been postulated to modulate the decrease in renal blood flow associated with cyclosporine nephrotoxicity. In particular, increases in renal production of the potent vasoconstrictor thromboxane A2 have been implicated in the pathogenesis of this disorder. The present study was undertaken to explore the relationship between alterations in urinary thromboxane B2 excretion (UTxB2V) and CsA nephrotoxicity in two rat models. Male Sprague-Dawley (SD) rats were treated for 14 days with CsA 50 mg/kg/day (n = 8) or olive oil (C) (n = 9) by gavage. Creatinine clearance (Ccr), urine flow (V), and urinary excretion rates of sodium, N-acetyl-beta-D-glucosaminidase (NAG), glucose, and TxB2 were determined before and after treatment. A similar study was conducted using Fischer rats (CsA: n = 10, C: n = 13). In Fischer rats, CsA caused a 35% decrease in Ccr (P = 0.01), a 33% decrease in sodium excretion (P = 0.02), and a greater than 2-fold increase in NAG excretion (P = 0.03), while V, glucose excretion, and UTxB2V did not change. Although similar changes in sodium and NAG excretion were seen after CsA administration in SD rats, Ccr was not affected. Additional findings in SD rats included a 3-fold increase in V (P less than 0.01), a 24-fold increase in glucose excretion (P = 0.03), and a 5-fold increase in UTxB2V (P = 0.04). Thus, Fischer rats developed CsA nephrotoxicity in the absence of increased UTxB2V. In contrast, SD rats failed to develop nephrotoxicity despite a marked increase in UTxB2V. We conclude that changes in renal TxA2 production are unrelated to the development of CsA nephrotoxicity.

Acetylglucosaminidase↗
PubMed1995

Chronic angiotensin-converting enzyme inhibition may improve sodium excretion in cardiac transplant hypertension.

Cyclosporine-associated hypertension (CAH) may be mediated in part by sodium and volume retention. To investigate this issue, we studied the effects of a calcium antagonist, nitrendipine (NIT, 10-20 mg b.i.d.), and a converting enzyme inhibitor, lisinopril (LIS, 10-20 mg o.d.), on blood pressure (office BP, 24 hr ambulatory BP), excretion of an acute sodium load (200 mmol/2 hr i.v.), glomerular filtration rate (insulin clearance), cumulative dopamine excretion, plasma atrial natriuretic peptide (ANP), and endothelin excretion in 8 patients with CAH after cardiac transplantation in a double-blind, randomized, crossover trial for 6 weeks. Five patients received a diuretic during the trial at a constant dose. Office diastolic BP (DBP) decreased significantly with LIS from 97 +/- 6 to 87 +/- 9 mmHg and with NIT from 96 +/- 7 to 92 +/- 12 mmHg. Ambulatory 24 hr DBP decreased significantly from 96 +/- 7 mmHg to 86 +/- 10 mmHg (LIS) and to 84 +/- 11 mmHg (NIT). Ambulatory DBP during the day was lowered significantly from 98 +/- 11 mmHg to 87 +/- 10 mmHg (LIS) and to 88 +/- 9 mmHg (NIT) and during the night from 95 +/- 9 mmHg to 86 +/- 8 mmHg (LIS) and to 79 +/- 7 mmHg (NIT). Cumulative sodium excretion 6 hr after an acute sodium load increased to 52 +/- 39 mmol (placebo), 96 +/- 44 mmol (LIS, P < 0.05 vs. placebo), and 71 +/- 34 mmol (NIT). Glomerular filtration rate, cumulative dopamine excretion, ANP, and endothelin excretion did not differ between either treatment group. We conclude, that: (1) both drugs were similar in lowering office BP and during the day, but NIT tended to be more effective during the night; and (2) cumulative sodium excretion during LIS was significantly increased compared with placebo. There was a similar trend during NIT also. Therefore, it is possible that chronic angiotensin-converting enzyme inhibition and possibly calcium antagonists might improve the sodium-retaining state in CAH independent of differences in blood pressure, ANP, dopamine, or renal function.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2004

Inhibition of both neutral endopeptidase and endothelin-converting enzyme by SLV306 reduces proteinuria and urinary albumin excretion in diabetic rats.

Diabetic nephropathy is a serious complication of diabetes associated with a poor prognosis which deteriorates to end-stage renal disease. Increased urinary excretion of protein and albumin are early clinical markers for diabetic renal disease and increased risk of cardiovascular disease. Diabetes causes activation of the renal endothelin system inducing renal damage. We analyzed the effects of SLV306, an inhibitor of both neutral endopeptidase and endothelin-converting enzyme, on diabetes-induced alterations of kidney function and morphology in rats with streptozotocin-induced diabetes. The effects of SLV306 (30 mg/kg per day), captopril (10 mg/kg per day), and placebo on urinary protein and albumin excretion as well as on blood pressure were studied in diabetic rats in comparison to non-diabetic control rats. The rats were treated for 20 weeks. At the end of the study kidney morphology was also analyzed using computer-aided image analysis systems. Serum glucose and blood pressure were similar in all diabetic groups. No side-effects were observed with SLV306 and captopril treatment. Protein excretion was 17.3 +/- 3.0 mg/24 hours in untreated diabetic rats. Protein excretion decreased significantly in the SLV306 (4.8 +/- 0.9 mg/24 hours; P = 0.03 vs untreated diabetic rats) as well as in the captopril (5.1 +/- 1.0 mg/24 hours; P = 0.03 vs untreated diabetic rats) -treated diabetic rats. Albumin excretion was 0.51 +/- 0.12 mg/24 hours in the untreated diabetic group and decreased likewise in the SLV306-treated diabetic rats (0.09 +/- 0.03 mg/24 hours; P = 0.04 vs untreated diabetic rats). The captopril-treated diabetic rats showed a strong trend towards reduced albumin excretion (0.12 +/- 0.04 mg/24 hours; P = 0.06 vs untreated diabetic rats). Computer-aided image analysis revealed that renal interstitial matrix content was significantly decreased in diabetic rats treated with either the angiotensin-converting enzyme inhibitor or the neutral endopeptidase/endothelin-converting enzyme inhibitor as compared to untreated diabetic rats. It was found that SLV306 decreases renal matrix protein content as well as protein and albumin excretion in diabetic rats independent of blood pressure. These effects are comparable to those of angiotensinconverting enzyme inhibition.

Administration, Oral↗
PubMed2003

Urinary protein and enzyme excretion as markers of tubular damage.

PURPOSE OF REVIEW: In this review we intend to evaluate the clinical usefulness of measurement of urinary excretion of microproteins and tubular enzymes. RECENT FINDINGS: Studies of patients with acute tubular necrosis showed that the excretion of some well known enzymes and of new markers such as kidney injury molecule-1 has higher value than classic renal function tests for the early detection of the disease as well as for the prediction of the development of overt acute renal failure. Tubular dysfunction may be detected by measurement of the excretion of tubular enzymes and microproteins not only in workers chronically exposed to heavy metals but also in population exposed to low environmental level below the limits set by the WHO. In chronic glomerulonephritis the excretion of alpha1-microglobulin is significantly associated with the extent of tubulo-interstitial damage and predicts outcome better than proteinuria/day; in the same diseases NAG excretion is significantly dependent on immunoglobulin G and alpha1-microglobulin excretion and predicts remission, progression and response to therapy. SUMMARY: The measurement of urinary excretion of tubular enzymes and microproteins may be clinically useful in several different kidney diseases (such as acute tubular necrosis, glomerulonephritis) both for diagnosis and prediction of fractional outcome.

Biomarkers↗
PubMed1983

Glycolate Formation and Excretion by Chlorella pyrenoidosa and Netrium digitus.

Conditions are described whereby suspensions of Chlorella pyrenoidosa and Netrium digitus photosynthetically biosynthesize and excrete glycolate continuously in high yields. Aminooxyacetic acid, an inhibitor of pyridoxal phosphate-linked enzymes, increased the excretion of glycolate approximately 4-fold in 1 hour (8 millimolar) and 20-fold in 4 hours (40 millimolar) in the presence of 0.2% CO(2) in air. The amount of glycolate excreted in the presence of aminooxyacetate and an atmosphere of 0.2% CO(2) in air equaled or exceeded the amount excreted in 0.2% CO(2) in O(2) minus aminooxyacetate. CO(2) and light were required for glycolate excretion. Aminooxyacetate also stimulated photosynthetic glycolate excretion in an atmosphere of 0.2% CO(2) in nitrogen or helium, although the stimulation was not as great as when air or O(2) was present.The excreted glycolate was converted to H(2) and CO(2) by the combined action of glycolic oxidase and the formic hydrogenlyase complex found in Escherichia coli in total conversion yields of 80%.

Journal Article↗
PubMed1988

Urinary excretion of 5-S-cysteinyldopa in relation to skin type, UVB-induced erythema, and melanocyte proliferation in human skin.

5-S-Cysteinyldopa (5-S-CD) is found in all pigment-producing cells and is the major precursor of phaeomelanin. However, the melanocyte specificity of the compound has been questioned. In order to elucidate the origin of 5-S-CD, we have now systematically studied the relationship between the 5-S-CD excretion in urine and the size of the melanocyte organ, UV-induced melanocyte proliferation, skin type, and the erythemal reaction. The skin type had no influence on the basal excretion of 5-S-CD. There was no significant correlation between the basal 5-S-CD excretion and the size of the melanocyte organ; that is, the number of skin melanocytes and nevi. During the irradiation, subjects with skin type II developed a more pronounced erythema (p less than 0.01) and had a significantly higher 5-S-CD excretion than those with skin type III-IV (p less than 0.01). No correlation was found between 5-S-CD excretion and UV-induced melanocyte proliferation. The lack of correlation between the basal 5-S-CD excretion and skin type or number of melanocytes suggests that the basal 5-S-CD in urine is mainly of extra-melanocytic origin. Our findings favor the view that the increase in 5-S-CD excretion during UV irradiation is due to UV damage.

Adult↗
PubMed1981

Effect of lactobacilli on urinary indican excretion in gnotobiotic rats and in man.

The effect of Lactobacillus species on urinary indican excretion in two types of gnotobiotic rats (GBH-9 and GB-5) and in man was studied. L. salivarius, L. plantarum and L. casei colonized in the cecum and colon of both types of rats at levels of 10(7) to 10(8) per gram of contents following one-dose oral administration and caused a significant reduction in urinary indican excretion, whereas two strains of L. acidophilus which colonized at low levels (10(4) to 10(5)/g) did not reduce indican excretion. Daily feeding of Lactobacillus concentrates caused a further significant reduction in indican excretion which was corrected by tryptophan intake, even in the case of L. acidophilus. There was a clear relationship between fecal lactobacillus counts and urinary indican. A significant reduction of indican secretion was obtained only when the fecal counts of lactobacilli exceeded 10(7).4/g in rats. L. casei also had an effect in man, reducing urinary excretion of indican and p-cresol. Reduction in indican excretion seems to be accompanied by decreasing fecal tryptophanase activity in rats and man. A negative correlation was also obtained between fecal resident lactobacilli and urinary indican in man (r = -0.532, n = 28, p less than 0.01). Subjects with lactobacilli at a level of 10(6)/g or more excreted less indican than those harboring the bacteria at levels below 10(5)/g.

Adult↗