Pentobarbital improves nitrogen retention in sepsis

Pentobarbital therapy has been associated with decreased urinary nitrogen excretion and resting energy expenditure in stressed patients. The metabolic effects of pentobarbital in sepsis were investigated in 29 well-nourished rats who underwent superior vena caval cannulation, cecal ligation, and puncture. Animals were randomly assigned to receive either a continuous infusion of 20 mg/kg/day of pentobarbital combined with parenteral nutrition (n = 13) or parenteral nutrition alone (n = 16). Both groups received isocaloric, isonitrogenous parenteral nutrition postoperatively for 24 hr. Mean nitrogen balance (+/- SEM) was better in the pentobarbital group (+169 +/- 76 mg/kg/day vs -190 +/- 66 mg/kg/day, p less than 0.01). No significant differences between the pentobarbital and control groups were noted for urinary 3-methylhistidine excretion (9 +/- 0.7 micrograms/kg/day vs 11 +/- 0.6 micrograms/kg/day, respectively) or 24 hr survival (77% vs 69%, respectively). Pentobarbital improves nitrogen retention without decreasing urinary 3-methylhistidine excretion in septic rats.     

Urea nitrogen excretion in chair-adapted primates

To evaluate the temporal pattern of urea excretion in chair-adapted primates (Macaque fascicularis) on continuous total parenteral nutrition (TPN), two groups of five animals were studied. Group I received continuous TPN (75 glucose kcal; 0.56 g nitrogen; and 100 ml fluid per kg per day) while Group II received a single morning isonitrogenous oral meal along with a continuous isovolemic intravenous infusion of 0.45% saline. Urine was collected hourly in group I for 2 days and every 4 hr in group II for 5 days and analyzed for urea content. Time series analysis revealed no periodicity of urea excretion in either group. Six animals were then studied for a total of 46 TPN days to define the relationship between the urea content of a single 3-hr morning urine aliquot and its respective content in a 24-hr collection. A significant linear relationship was found (r = +0.76, p less than 0.01). However, using this relationship, a reasonable estimate (+20%) of measured 24-hr urea output was achieved only 50% of the time using a single 3-hr urea output. Chair-adapted primates maintained on continuous TPN or a single oral meal with continuous saline infusion do not exhibit a periodic pattern of urea excretion. The variability in 3-hr urinary urea output in the chaired primate on continuous TPN does not consistently permit accurate estimation of the coincident 24-hr urinary urea output.     

Diagnostic chelation challenge with DMSA: a biomarker of long-term mercury exposure?

Chelation challenge testing has been used to assess the body burden of various metals. The best-known example is EDTA challenge in lead-exposed individuals. This study assessed diagnostic chelation challenge with dimercaptosuccinic acid (DMSA) as a measure of mercury body burden among mercury-exposed workers. Former employees at a chloralkali plant, for whom detailed exposure histories were available (n = 119), and unexposed controls (n = 101) completed 24-hr urine collections before and after the administration of two doses of DMSA, 10 mg/kg. The urinary response to DMSA was measured as both the absolute change and the relative change in mercury excretion. The average 24-hr mercury excretion was 4.3 microg/24 hr before chelation, and 7.8 microg/24 hr after chelation. There was no association between past occupational mercury exposure and the urinary excretion of mercury either before or after DMSA administration. There was also no association between urinary mercury excretion and the number of dental amalgam surfaces, in contrast to recent published results. We believe the most likely reason that DMSA chelation challenge failed to reflect past mercury exposure was the elapsed time (several years) since the exposure had ended. These results provide normative values for urinary mercury excretion both before and after DMSA challenge, and suggest that DMSA chelation challenge is not useful as a biomarker of past mercury exposure.     

Biological monitoring of human exposure to acephate

Acephate is a water-soluble organophosphate insecticide whose action on insects has been related to its conversion to methamidophos, a very potent anticholinesterase agent which has caused delayed neuropathy in man.Inhalation and skin exposure to acephate was evaluated in four workers engaged in 8-day campaigns with the formulation of the 97%-pure technical product. Before, during, and after exposure, the workers were monitored for the urine content of acephate and methamidophos, and for erythrocyte (AChE) and plasma (PChE) cholinesterase levels. Median air concentrations (8-hr TWA) ranged from 0.278 to 2.170 mg/m³; median total-body skin deposition ranged from 26.1 to 41.9 mg/day. Based on these values, daily workers' absorption of acephate was estimated to be in the order of 10–20 mg. Urinary excretion of unchanged acephate followed a pattern consistent with exposure, showing peak values of excretion during the workshift or in the eight hr after the end of the workshift. The urine levels of unchanged acephate were found to vary from 1 to 10 mg/L. Methamidophos was not detected in any urine sample (detection limit: 30 u.g/L). High correlation (r=0.78) was found between skin exposure level and urine acephate elimination. No changes in AChE or PChE were observed for the workers whose urinary concentrations of acephate were 1 or 2 mg/L. One subject who had urinary acephate excretion between 3 and 8 mg/L, showed slightly decreased values of PChE during exposure and of AChE after exposure.     

北京市成人雌马酚代谢水平及健康效应

目的 确定北京市成人雌马酚等大豆异黄酮代谢水平,分析雌马酚表型与血脂、尿酸等健康指标的关系。方法 应用现况调查方法,调查北京市区180名20～72岁健康志愿者生活方式及膳食营养素摄入量;采用高压液相色谱(HPLC)法分析负荷大豆异黄酮前后尿中雌马酚等代谢物24h排泄量,分析雌马酚表型与血脂、血尿酸等健康指标的关系。结果 基线调查中,产雌马酚者48人,占26.7%,其中男女性各24人,分别占男女性总数的26.7%,经χ²检验,差异无统计学意义(P>0.05):产雌马酚者的体质指数(BMI)为(23.33±3.21)kg/m²,与非产雌马酚者为(23.59±3.04)kg/m²2者比较,差异无统计学意义(P>0.05);产雌马酚者膳食大豆蛋白和大豆异黄酮摄入量与雌马酚排泄量呈正相关(r=0.47,0.46,P<0.01),而非产雌马酚者无相关性(P>0.05);大豆异黄酮负荷试验中,产雌马酚者104人,占57.8%;其中男性50人,占男性总数的55.6%,女性54人,占女性总数的60.0%,经χ²检验,差异无统计学意义(P>0.05)。结论 180名健康志愿者有较高的潜在产生雌马酚能力;雌马酚代谢表型具有潜在的保护心血管疾病作用。     

猕猴桃浓缩果汁中抗坏血酸在人体的利用

中华猕猴桃是我国的特产野果。鲜果中抗坏血酸含量一般在50～400mg/100g,最高可达2000mg/100g。制成浓缩汁后含量约为350～400mg/100ml。为观察其浓缩果汁中抗坏血酸的利用做了人体实验。受试者为9名男大学生,年龄19～23岁,平均体重56.0kg,身长166.6cm。实验分四期,第一及第三期为抗坏血酸饱和期;第二期为十天的对照期,食基础膳,以晶体抗坏血酸补足至每人每日摄入总量为75mg;第四期为十天的实验期,食基础膳,以猕猴桃汁补充抗坏血酸使每日每人摄入总量亦为75mg。对照期及实验期最后三天收集空腹1小时及24小时尿,最后2天取空腹血浆,皆用靛酚滴定还原型抗坏血酸含量。利用率系以实验期尿中排出率与对照期尿中排出率的比值而求得。算出猕猴桃汁中抗坏血酸利用率为94％。对照期及实验期最后三天24小时尿抗坏血酸排出分别为 20 1±1.63及18.8±1.22mg;空腹1小时尿分别为0.94±0.07及0.75±0.07mg。空腹血浆分别为0.83±0.04及0.81±0.02mg/100ml。分别作t试验,皆无显著性差异。并可看出每日供给75mg抗坏血酸可满足男大学生的需要,与以往报告基本一致。     

Intramuscular administration of ACTH1-24 vs. 24-hour blood sampling in the assessment of adrenocortical function

The standard intravenous short Synacthen test (SSST) has long been accepted as one of the most reliable diagnostic tests of adrenocortical insufficiency. Intramuscular (i.m.) administration of ACTH obviates the need of venous cannulation and can be used as an alternative to the intravenous test. Nevertheless, reports of correlation between cortisol response to i.m. ACTH1-24 and 24-hr average cortisol concentration are scarce. We studied this relation in 64 nonobese healthy men. Blood samples for serial cortisol measurements were collected hourly over 24 hrs. The following day, blood samples were collected at baseline and at 30 and 60 min after intramuscular (i.m.) administration of 250 microg of ACTH1-24. All healthy men reached 24-hr serum cortisol peak values (Cmax) between 0600 h and 1000 h. Following i.m. ACTH1-24, cortisol levels significantly increased at both 30 (C30ACTH) and 60 (C60ACTH) minutes, when compared to baseline values. C30ACTH and C60ACTH significantly correlated with Cmax and with the 24-hr time-integrated cortisol concentration (AUC0-24). Morning mean cortisol was calculated as the average of serum concentrations measured between 0600 h and 1000 h (C(av)6-10) and correlated very well with AUC0-24. In conclusion, we confirmed that i.m. administration of ACTH1-24, followed by a single blood sampling at 60 min for cortisol measurement represents a valid, convenient and cost- effective screening test of adrenal function.     

Pantothenic acid status of adolescents

Information on human needs for pantothenic acid is limited and no recommended daily allowance has been established, although a safe and adequate level of 4-7 mg/day has been suggested for adults and adolescents. Pantothenic acid levels in urine, whole blood, and erythrocytes were determined by radioimmunoassay in 63 healthy adolescents. Dietary intakes were calculated and evaluated from 4-day diet records. Although 49% of the females and 15% of the males consumed less than 4 mg/day, average blood levels for both groups were in a normal range relative to other populations (411.9 +/- 102.8 ng/mL and 344.5 +/- 113.6 ng/mL, respectively). Dietary intake was highly correlated with urinary excretion (p less than 0.001). Levels of pantothenic acid in erythrocytes correlated well with dietary intake and urinary excretion. A model was developed to predict circulating levels of pantothenic acid from dietary intake and urinary excretion.     

Inhibition of liver, kidney, and erythrocyte delta-aminolevulinic acid dehydratase (porphobilinogen synthase) by gallium in the rat

Selective inhibition of enzymes in the heme biosynthesis pathway with concomitant urinary excretion of heme precursors serve as potentially important biological markers of chemical exposure and cell injury. Intratracheal administration of gallium arsenide particulate suspensions has been shown to result in inhibition of delta-aminolevulinic acid dehydratase (ALAD) in several tissues and increased excretion of the heme precursor aminolevulinic acid (ALA). This study was undertaken to evaluate in vivo the role of gallium alone in ALAD inhibition and increased urinary excretion of ALA. Male CD rats received a single ip injection of Ga2(SO4)3 at doses of 12.5, 25, 50, 100, and 200 mg Ga/kg. A dose-dependent inhibition of ALAD was observed 24 hr later in liver, kidney, and erythrocytes. After injection of 25 mg Ga/kg, maximal inhibition (42 to 49% of control) of ALAD occurred between 6 and 24 hr in liver and kidney with full recovery of activity at 96 hr. In erythrocytes, maximal inhibition (48% of control) occurred between 24 and 48 hr with recovery of activity at 96 hr. Mild to moderate renal proximal tubular necrosis in the pars recta was observed 24 hr after administration of 100 and 200 mg/kg, but no histopathologic changes were evident at lower doses. No consistent changes in urinary excretion of ALA were observed. Lineweaver-Burk analyses of renal and hepatic ALAD activities in the absence and presence of gallium indicated that the inhibition of ALAD by this element is noncompetitive (same Km, decreased Vmax). Gallium was shown to possess an inhibition constant (Ki) of approximately 3 microns for ALAD, similar to the Ki obtained for lead in other studies. Incubation of ALAD in vitro with gallium and lead, an active thiol group inhibitor, resulted in a greater inhibition of the enzyme. Further in vitro studies demonstrated the attenuation of gallium inhibition of hepatic and renal ALAD by zinc, suggesting that the mechanism of gallium action may involve competition for or displacement of zinc from the sulfhydryl group of the enzyme active site. Since ALAD inhibition occurred at doses at which no histopathologic changes were evident, the determination of ALAD activity in various tissues, including blood, may be of potential value as a biomarker of exposure/toxicity to metals such as gallium. The effect of chemical form and route of exposure of gallium and effects of other Group III metals on inhibition of ALAD and excretion of ALA is discussed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Transperitoneal absorption of intralipid in rats: total serum fatty acids and triglyceride after absorption

Intralipid 20% was injected percutaneously into the peritoneum of 58 female rats. The rats were divided into seven groups (with an additional control group of 35 rats). To measure transperitoneal absorption, we determined the serum fatty acid and triglyceride concentrations at 3-hr intervals for 24 hr, and found a considerable increase in all of the levels measured, with a maximum at about 6 hr. The serum triglyceride levels never rose above a mean value of 200 mg/100 ml. A second and smaller rise was seen after 15 hr, declining again to the initial values. The relative proportions of the different fatty acids changed, but not drastically.     

Magnesium, zinc, and copper status in women involved in different sports

The dietary intake, serum levels, and urinary excretion of magnesium, zinc, and copper were studied in 78 women involved in different sports (karate, handball, basketball, and running) and in 65 sedentary women. Seven-day, weighed-food dietary reports revealed that no group of female athletes reached the minimal intake recommended for magnesium (280 mg/day) and zinc (12 mg/day), although their values were superior to those of the control group. The estimated safe and adequate minimal intake of copper (1.5 mg/day) was amply surpassed by the basketball players and runners but was not reached by the handball players. Serum levels and urinary excretion of magnesium, zinc and copper di not seem related either to their intake or to the type of physical activity performed. The influence of other factors such as nutritional status, bioavailability, intestinal absorption mechanisms, and muscle-level modifications might explain the differences between the different groups of female athletes.     

EXCRETION OF MALONDIALDEHYDE, FORMALDEHYDE, ACETALDEHYDE AND ACETONE IN THE URINE OF RATS FOLLOWING ACUTE AND CHRONIC ADMINISTRATION OF ETHANOL

Recent studies have shown that xenobiotics which induce oxidativeStress result in an increased production and excretion of acetaldehyde(ACT), formaldehyde (FA), acetone (ACON) and malondialdehyde(MDA) in the urine of rats. We have therefore examined the effectof acute and chronic ethanol administration on the excretionof these four lipid metabolites in female Sprague-Dawley rats.Urine samples were collected over dry ice for 6 hr time periods.Aliquots of urine were derivatized with 2,4-dinitrophenylhydrazineHCl, and extracted with n-pentane. High pressure liquid chromatography(HPLC) was used to quantitate and the hydrazones of the fourlipid metabolite products. Following a single, oral, acute doseof 5 g ethanol/kg, urinary excretion of ACT increased approximately5.8-fold from 6 to 12 hr post-treatment, and decreased thereafter.FA excretion decreased by approximately 50% from 0 to 12 hr,returned to control values in the 18–24 hr urine samples,and was 1.3-fold greater than control values at 42–48hr. ACON increased 3.1-fold over control values from 0 to 30hr and remained elevated throughout the remaining 18 hr of thestudy. The excretion of MDA increased approximately 1.5-foldfrom 18 to 36 hr, then remained constant through the 48 hr timepoint. In a separate series of experiments, a chronic oral doseof 0.5 g ethanol/kg was administered to rats for 10 consecutivedays and the urinary excretion of the lipid metabolites MDA,FA, ACT and ACON was examined for 11 days, beginning with thefirst day of ethanol administration. During the chronic administrationof ethanol, a significant increase in the urinary excretionof ACT began on day 4. An increase in ACON excretion was firstobserved on day 6, and increases in MDA and FAexcretion werefirst observed on days 8 and 10, respectively. The results clearlydemonstrate that both acute and chronic alcohol consumptionmarkedly afier lipid metabolism and the excretion of lipid metabolites.     

Comparison of urinary urea nitrogen excretion and measured energy expenditure in spinal cord injury and nonsteroid-treated severe head trauma patients

Severe head trauma patients (HT) exhibit markedly elevated energy expenditure and 24-hr urinary urea nitrogen excretion (UUN) values. The objective of this study was to compare seven spinal cord injured patients (SCI) to seven HT for changes in UUN and measured energy expenditure (MEE) over the first 18 days following injury. Energy expenditure was measured by indirect calorimetry and compared to values predicted by the Harris Benedict Equation (PEE). There were six quadriplegics and one paraplegic in the SCI group. HT patients had peak Glasgow Coma Scale scores of 3 to 10 for the first 24 hr postinjury. Patients were studied prospectively and matched for age, sex, and admitting weight Week 1 following the injury, SCI had mean UUN values of 0.18 +/- 0.04 g/kg/day vs 0.18 +/- 0.01 for HT patients. The mean MEE/PEE ratio was 0.56 for the SCI and 1.4 for HT (p less than 0.01). Over the entire study period the mean UUN value for SCI was 0.23 +/- 0.03 g/kg vs 0.21 +/- 0.01 for HT. The mean MEE/PEE ratio for SCI was 0.94 while HT remained elevated at 1.5 (p less than 0.05). Although the UUN was comparable in SCI vs HT, there was a significant difference in MEE/PEE between the groups. The elevation in UUN observed in SCI is not due to a hypermetabolic state. This suggests that different mechanisms promote the increased nitrogen excretion observed in these two populations.     

Inhalation exposure to 1,3-dichloropropene in the Dutch flower-bulb culture. Part II. Biological monitoring by measurement of urinary excretion of two mercapturic acid metabolites

A biological monitoring study was carried out in the Dutch flower-bulb culture to determine the relationship between respiratory occupational exposure to Z- and E-1,3-dichloropropene (Z- and E-DCP) and urinary excretion of two mercapturic acid metabolites, N-acetyl-S-(Z- and E-3-chloropropenyl-2)-L-cysteine (Z- and E-DCP-MA). Urinary excretion of Z- and E-DCP-MA, either based on excretion rates or on creatinine excretion, followed first order elimination kinetics after exposure. Urinary half-lives of elimination were 5.0 ± 1.2 hr for Z-DCP-MA and 4.7 ± 1.3 hr for E-DCP-MA and were not statistically significantly different. Calculated coefficients of variation indicated that the half-lives of elimination of Z- and E-DCP-MA were quite consistent inter- and intra-individually.Strong correlations (r 0.93) were observed between respiratory 8-hr time weighted average (TWA) exposure to Z-and E-DCP and complete cumulative urinary excretion of Z- and E-DCP-MA. Z-DCP yielded three times more mercapturic acid than E-DCP, probably due to differences in metabolism. Z- and E-DCP were excreted 45 and 14% as their respective mercapturic acid metabolites.A respiratory 8-hr TWA exposure to the Dutch occupational exposure limit of 5 mg · m^–3 DCP would result in a complete cumulative excretion of 14.4 mg (95% confidence interval: 11.7–17.0 mg) Z-DCP-MA and 3.2 mg (95% confidence interval: 2.3–4.1 mg) E-DCP-MA.     

Exposure of apple thinners to parathion residues

In studies of potential exposure of a volunteer working under controlled conditions during apple hand-thinning operations at 1, 24, 48, 72, 96, 168, and 240 hr after application of conventional 0.03% parathion spray, both dermal and respiratory exposure values were greater where water-wettable powder formulations were used than where emulsifiables were used. Residue levels of parathion on leaves from the two types of applications were about the same. Only trace amounts of paraoxon could be detected at one and seven days after application. Highest exposure values (14.2 mg/hr dermally and 0.15 mg/hr respiratorily) were obtained within 24 hr of application. Exposure was considerably less after residues were 72 hr old. Greatest exposure was on the forearms and hands. Urinaryp-nitrophenol excretion indicated slightly more absorption following exposure in water-wettable powder experimental plots. Potential exposure values indicate that absorption could reach hazardous levels after one or two hr of work, even at the 96-hr residue period, if all the pesticide were absorbed. Considering that only a small fraction of the total amount would be absorbed, it is calculated that at 72-hr residue period poisoning should not occur. There was no significant change in blood cholinesterase activity of the volunteer worker. Variation in spray deposit within an orchard due to poor tank mixing did not appear to be great enough to be considered an important factor affecting exposure.     

On supplementing the selenium intake of New Zealanders. 2. Prolonged metabolic experiments with daily supplements of selenomethionine, selenite and fish

1. The daily intake of selenium by three subjects was supplemented with 100 microgram Se as selenomethionine (Semet-Se) or sodium selenite (selenite-Se)/d for 10-11 weeks, or with 65 microgram Se as in mackerel (Scomber japonicus) (fish-Se)/d for 4 weeks. 2. Urinary and faecal excretion of Se was measured and also Se concentration in whole blood, plasma and erythrocytes. Measurements on blood were made at intervals after supplementation had ceased. 3. Selenite-Se was not as well absorbed (0.46 of the intake) during the first 4 weeks as Semet-Se (0.75 of the intake) and fish Se (0.66 of the intake). 4. Blood Se increased steadily with Semet-Se, from 0.08 to 0.18 microgram Se/ml, but more slowly with selenite-Se, reaching a plateau in 7-8 weeks at 0.11 microgram Se/ml. Plasma Se increased more rapidly with Semet-Se than with selenite-Se, so that initially with Semet-Se plasma Se was greater than erythrocyte Se. 5. Daily urinary excretion increased with all forms of supplement, with initially a greater proportion of absorbed selenite-Se being excreted than Semet-Se or fish-Se. A close relationship was found between plasma Se and 24 h urinary excretion. The findings suggested that there was a rapid initial excretion of presumably unbound Se then a slower excretion of residual unbound, loosely bound or bound Se. 6. Total retentions of 3.5 mg selenite-Se and 4.5 mg Semet-Se were large when compared with an estimate of body content of 6 mg Se, derived in another paper (Stewart, Griffiths, Thomson & Robinson, 1978). Retention of Semet-Se and fish-Se appeared to be reflected in blood Se, whereas for selenite-Se, blood Se reflected retention for only a short period after which Se appeared to be retained without altering the blood Se. This suggested that Semet-Se and selenite-Se were metabolized differently. 7. A double blind-dosing trail with 100 microgram Semet-Se was carried out for 12 weeks on twenty-four patients with muscular complaints in Tapanui, a low-Se-soil area. Blood Se increased in the experimental group (from 0.067 to 0.143 microgrm Se/ml); clinical findings were not conclusive and will be presented elsewhere. 8. Bood Se was measured in New Zealand residents before travelling to Europe or to North America. On return their blood Se was increased, and depending upon the period of time spent outside New Zealand some values reached concentrations found in visitors and new settlers to New Zealand. 9. The results from these studies and the earlier studies of single and multiple dosing have been used to look at the various criteria in use for assessing Se status of subjects. It is suggested that plasma Se be used in preference to 24 h urinary excretion, and in addition to whole blood Se and glutathione peroxidase (EC 1.11.1.9) activity.     

A biomonitoring procedure utilizing negative phototaxis of first instarAedes aegypti larvae

Negative phototaxis of newly hatchedAedes aegypti L. larvae was inhibited by exposure to three heavy metals and five organic insecticides. This response was quantified in an inexpensive multiunit apparatus consisting of four glass troughs perpendicular to a uniform light source. The criterion of toxic effect, established with cupric sulfate as a standard, was: inability of larvae to migrate 30 cm in 60 sec after 8 hr of pre-exposure, designated as 8-hr EC₅₀. The photomigration procedure was more sensitive than our comparative 24-hr acute lethal toxicity tests on metals. The 8-hr EC₅₀ values for cadmium, chromium and copper were 0.6, 2.4, and 1.4 mg/L, respectively. Values for insecticides ranged from 0.003 mg/L for fenitrothion (organophosphate) to 0.39 mg/L for methomyl (carbamate).     

Metabolic balances of cadmium, copper, manganese, and zinc in man.

Balance studies of cadmium, copper, manganese, and zine were carried out under constant dietary conditions in eight adult males during two calcium intake levels of 200 and 800 mg/day and in an additional single case during a calcium intake of 1500 mg/day. The dietary content and the excretions of these elements in urine and stool were determined. The mean dietary content of cadmium was 32.9 micrograms/day, of copper 1020 micrograms/day, of manganese 2130 micrograms/day, and of zinc 12.4 mg/day. The ratio of the fecal/urinary cadmium excretion was approximately 1.5 and the main pathway of excretion of the other three elements was via the intestine, while the urinary excretions were very low. The different trace element balances were either slightly negative or in equilibrium, except that the zinc balances was positive in 50% of the cases. All balances should be considered maximal values, as the losses in sweat were not determined. The calcium intake level had little effect on the excretion and retention of these trace elements.     

Urinary monitoring method of 3,3'-dichlorobenzidine (DCB) and its metabolites,N-acetyl-DCB and N,N'-diacetyl-DCB

3,3'-dichlorobenzidine (DCB) is suspected to be arcinogenic in experimental animal and human. Several studies have investigated excretion of metabolites in urine, hemoglobin adduction and cancer incidence among workers exposed occupationally to DCB. In these researches, metabolites of DCB had a very important role. The purpose of this study was to develop the urinary monitoring method of its metabolites from rats exposed with DCB, by easily synthesizing them in the laboratory. N,N'-diacetyl-DCB was easily synthesized with DCB in pyridine by adding sufficient acetyl chloride or acetic anhydride. N-acetyl-DCB was isolated from the supernatant, which made by adding 21/microl acetyl chloride (more 3 times than DCB in moles) to 32 mg DCB in 2 ml pyridine and 0.3 ml acetic acid. Gas chromatography/mass spectrometry (GC/MS) was used for the identification, gas chromatography nitrogen phosphorous detection (GC-NPD) for the quantification and gas chromatography flame ionization detection (GC-FID) for the determination of purity. The base peak of DCB, N-acetyl-DCB and N,N'-diacetyl-DCB was 252 m/z. The other main peaks were 294 m/z for N-acetyl-DCB, and 294 and 336 m/z for N,N'-diacetyl-DCB. The purities of N-acetyl-DCB and N,N'-diacetyl-DCB were identified as 98.82 and 98.72% by GC-FID, respectively. After treatment orally to rats with 20 mg DCB/kg body weight for 2 weeks, the urinary excretion amount of DCB was nearly constant at range of 0.11-0.18 mg/L for 2 weeks. But excretion of N-acetyl-DCB was continually increased from 1.30 mg/L on 1st day to 4.15 mg/L on 14th day. And level of N,N'-diacetyl-DCB in urine was sharply increased from 2.13 mg/L on 1st day to 11.00 mg/L on 14th day.     

Hydroxyproline excretion in urine of smokers and passive smokers

Urinary hydroxyproline excretion was investigated in 125 male cigarette smokers, 194 male pipe and/or cigar smokers, and 24 male nonsmokers. Hydroxyproline excretion was calculated either as hydroxyproline/creatinine ratio or as body surface-standardized amounts of hydroxyproline excreted in urine sampled during day, during night, or over 24 hr. The association of hydroxyproline excretion with smoke uptake variables such as daily cigarette consumption, carboxyhemoglobin, serum cotinine, and nicotine in urine and with self-reported passive smoking exposure in nonsmokers was analyzed. The hydroxyproline/creatinine ratio was found to be unsuitable as a measure of hydroxyproline excretion since creatinine urine concentrations correlate inversely with smoke uptake in cigarette and pipe/cigar smokers. The amount of hydroxyproline excreted in 24-hr urine and standardized for body surface was not significantly associated with smoke uptake in pipe/cigar smokers or exposure to passive smoking in nonsmokers. In cigarette smokers the situation appeared similar, although the results were less clear-cut. The data do not favor the premise that measuring urinary hydroxyproline excretion is an accurate method of investigating a lung-damaging effect of smoking, passive smoking, or air pollution.