• Journal of Preventive Medicine and Public Health
• /
• v.13 no.1
• /
• pp.27-34
• /
• 1980

Purpose of this study is to find out proper means of estimating the urinary mercury excretion in the normal individuals. Whole void volume was collected every 2 hours beginning from 6 o'clock in the morning until 6 o'clock next morning. Mercury excretion in each urine specimen was measured by NIOSH recommended dithizone colorimetric method (Method No.: P & CAM 145). Urinary concentration of mercury was adjusted by two means: specific gravity of 1.024 and a gram of creatinine excretion per liter of urine comparing the data with the unadjusted ones. Mercury excretion in 24-hour urine specimen was calculated by adding the amounts measured with the hourly collected specimens of each individual. Statistical analysis of the urinary mercury excretion revealed the following results: 1. Frequency distribution curve of mercury excreted in urine of hourly specimens was best fitted to power function expressed in the form of $y=ax^b$. Adjustment of the urinary mercury concentration by creatinine excretion was shown to be superior($y=1674x^{-1.52},\;r^2=0.95$) over nonadjustment($y=2702x^{-1.57},\;r^2=0.92$) and adjustment by specific gravity of 1.024($y=4535x^{-1.66},\;r^2=0.93$). 2. Both log-transformed mercury excretion in hourly voided specimens and mercury excretion itself in 24 hour specimens showed the normal distributions. 3. The frequency distribution of mercury adjusting the urinary concentration of mercury by creatinine excretion was best fitted to a theoretical normal distribution with the sample means and standard deviation than those unadjusted or adjusted with specific gravity of 1.024. 4. Average urinary mercury excretions in 24-hour urine specimen in an individual were as follows: a) Unadjusted mercury excretion mean and standard deviation : $$18.6{\pm}13.68{\mu}gHg/l$$. median : $$16.0\;{\mu}gHg/l$$. range : $$0.0-55.10\;{\mu}gHg/l$$. b) Adjusted with specific gravity mean : $$20.7{\pm}11.76\;{\mu}gHg/l{\times}\frac{0.024}{S.G-1.000}$$ median : $$20.7\;{\mu}gHg/l{\times}\frac{0.024}{S.G-1.000}$$ range : $$0.0-52.9\;{\mu}gHg/l{\times}\frac{0.024}{S.G-1.000}$$ c) Adjusted with creatinine excretion mean and standard deviation : $$10.5{\pm}6.98\;{\mu}gHg/g$$ creatinine/l median : $$9.4\;{\mu}gHg/g$$ creatinine/l range : $$0.0-26.7\;{\mu}gHg/g$$ creatinine/l 5. No statistically significant differences were found between means calculated from 24-hour urine specimens and those from hourly specimens transformed into logarithmic values. (P<0.05).

• Analytical Science and Technology
• /
• v.24 no.3
• /
• pp.183-192
• /
• 2011

This study was done for the determination and excretion profile of superdrol and its metabolites in human urine using both liquid chromatography with electrospray ionization mass spectrometry and gas chromatography with mass spectrometry after trimethylsilylation. Superdrol and its two metabolites were detected in human urine after administration of superdrol to healthy volunteers. The intra-day recovery ranged 89.7-113.2%, accuracy ranged 91.8-113.8% and reproducibility ranged 0.2-6.8% and inter-day recovery ranged 89.3-104.1%, accuracy ranged 95.2-103.0%, reproducibility ranged 0.7-7.8%. We found that superdrol M1 was a hydration at C-3 and superdrol M2 was a hydroxylation at D-ring. Superdrol and two metabolites were excreted as their glucuronided fractions. The glucuro-/sulfa-conjugated ratio of superdrol, superdrol M1 and superdrol M2 were 0.02, 0.02, 0.01, respectively. The excretion studies showed that superdrol and two metabolites were reached 4.3 h after oral administration and superdrol and superdrol M1 were detected until 48 h in human urine.

• YAKHAK HOEJI
• /
• v.29 no.3
• /
• pp.130-143
• /
• 1985

Bumetanide, when given intravenously in dogs, induced a potent diuresis with an increased amounts of sodium and potassium excreted in urine due to inhibition of reabsorbing them in renal tubule. Furthermore, clearances of osmolar substance and para-aminohippuric acid were increased, but clearace of free water diminished without any change of creatinine clearance. Bumetanide, administered directly into a renal artery, elicited diuresis only in the infused(experimental) kidney by the same mode of action as in the intravenous cases in renal function of the dog. Renal effects of intravenous bumetanide after pretreatment with the small dose of indomethacin (5.0mg/kg) revealed reduction only in clearance of paraaminohippuric acid. However the much dose of indomethacin (5.0mg/kg+5.0mg/kg/hr) or arachidonic acid showed a significant inhibition in the change rates of all renal function by bumetanide. Morover, pretreatment of probenecid also made a marked reduction in renal effects induced by bumetanide. From the above results, it is thought that bumetanide causes diuretic action due to dual mechanism inhibiting reabsorption of electrolytes in loop of Henle and increasing blood flow in kindney, that are provoked through the mediation of prostaglandins.

• Biomolecules & Therapeutics
• /
• v.1 no.2
• /
• pp.204-210
• /
• 1993

The distribution and excretion of DWC-751, a new cephalosporin, were examined in rats and mice following a single intravenous administration. DWC-751 in plasma and urine was determined by both HPLC and microbiological assay. The plasma concentration of the drug declined biexponentially. The initial and terminal half lives of the drug were 3.0 and 28.3 min, respectively. Binding of the drug to plasma proteins was 42.3%. The distribution volume at steacly-state ($Vd_{ss}$) was only 0.341 ι/kg, which is well correlated with the low n-octanol/water partition coefficient of the drug ($K_{o/w{\cong}0$) Actually, the drug was distributed to liver, kidney and lung with very low organ/plasma concentration ratio. The drug, was excreted mainly via renal excretion, i.e., the total($CL_T$) and apparent renal($CL_{R}$) clearances of the drug were 10.8 and 7.5 ml/min/kg, respectively.

• Journal of Nutrition and Health
• /
• v.27 no.10
• /
• pp.1037-1047
• /
• 1994

Dietary iodine intake and urinary iodide excretion were meassured from 110 patients with various thyroid hormone diseses(hypothyroidism, hyperthyroidism, simple goiter and thyroid adenoma) and 67 normal control subjects. Iodine intake was assessed on the 24-hour recall dietary data using the compiled lists of food iodine values developed from various countries. Urinary iodide concentrations of drink water samples were measured with the iodide-selective electrode. The average iodine intake of the thyroid patients was 411$\mu\textrm{g}$, which was 87% higher(p<0.05) than that of the control subjects(220$\mu\textrm{g}$). Patients with hyperthyroidism and hypothyroidism or simple goiter excreted the most(0.6442ppm) amount of iodide respectively in the urine, with the control subject in the middle(0.5229ppm). Iodide concentrations of the drinking water samples were found to be in the range of 0.0015ppm to 0.0214ppm, which seemed to vary depending on the kind(underground water vs public water) and the location.

• Journal of Environmental Health Sciences
• /
• v.40 no.4
• /
• pp.294-303
• /
• 2014

Objectives: Excretion and tissue distribution of titanium oxide nanoparticles were evaluated in rats after oral administration. The relation between toxicity and systemic concentration of nanoparaticles was investigated. Methods: Rats were orally treated with titanium oxide nanoparticles (10, 100 mg/kg) for five consecutive days. General toxicity, blood chemistry, and serum biochemical analysis were analyzed. Titanium concentration in liver, kidney, lung, urine and feces were measured and histopathology was performed in these organs. Results: Induction of toxicological parameters was not observed and titanium nanoparticles were excreted via feces. Conclusion: Absorption of titanium oxide nanoparticles via the gastrointestinal tract after oral administration was very poor and systemic concentration of titanium oxide nanoparticles was not elevated. Titanium oxide nanoparticles did not cause toxicities in rats after oral administration.

• Biomolecules & Therapeutics
• /
• v.3 no.2
• /
• pp.136-142
• /
• 1995

This study was performed in order to certify the antidiuretic action and to investigate the mechanism of antidiuretic action of debrisoquin infused into a renal artery in dog. Debrisoquin, when infused into a renal artery, exhibited the antidiuretic action accompanied the reductions of glomerular filtration rate and renal plasma flow, and the decreased amounts of sodium and potassium excreted in urine, limited only to the infused side, while control kidney function remained unchanged at all. The antidiuretic action of debrisoquin infused into a renal artery was blocked by pretreament of prazosin, $\alpha$$_1$-adrenergic blocking agent, or reserpine, catecholamine depleting agent. These results suggest that debrisoquin infused into a renal artery elicits antidiuretic action through indirect stimulation of renal sympathetic nerves.

• Biomolecules & Therapeutics
• /
• v.1 no.1
• /
• pp.84-92
• /
• 1993

This study was performed to elucidate the mechanism of antidiuretic action of diltiazem by infusion into the vein and carotid artery, of diuretic action into a renal artery in dog. Renal denervation caused a reversal of the effect of diltiazem from the antidiuretic to the diuretic when infused into vein or carotid artery, and potentiated the diuretic effect when infused into a renal artery. The changes of renal function in diuretic circumstances as described above included the increase in renal plasma flow, osmolar clearance, the amounts of sodium and potassium excreted in urine and the decrease in reabosrption rate of sodium and potassium in renal tubules. Above results suggest that antidiuretic action of diltiazem may be mediated by central nervous system, not by endogenous substance, diuretic action by direct renal action.

• YAKHAK HOEJI
• /
• v.28 no.3
• /
• pp.149-160
• /
• 1984

In order to certify the diuretic mechanism of dopamine, this study was performed in dog. The following results were obtained. Dopamine, when given intravenously, produced diuresis, and increased glomerular filtration rate (GFR), renal plasma flow (RPF), and amount of sodium excreted in urine. When infused directly into a renal artery, dopamine elicited a marked diuresis confined only to the infused side, with concomitant rises in osmolar clearance and sodium excretion as well as a slight increase in free water clearance. Simultaneously total renal plasma flow and medullary plasma flow increased markedly with a increase of glomerular filtration rate and renal plasma flow. Medullary concentration gradient of sodium also markedly lowered in the infused kidney. These changes were not observed during mannitol diuresis and renal action of dopamine were not apparent in dog pretreated with haloperidol. From the above experimental results, it is thought that dopamine, when given into a vien or infused directly into a renal artery, induces diuresis, and the mechanism of its action is due to dual actions which are hemodynamic effect along with glomerular filtraction rate, and the increased response in the medullary blood flow.

• Archives of Pharmacal Research
• /
• v.13 no.2
• /
• pp.147-150
• /
• 1990

Methotrexate (MTX)-poly-L-lysine (PLL) conjugate was relatively stable in phosphate buffer of pH 7.4 and in plasma. However, liver homogenate accelerated the release of MTX from the conjugate. Pharmacokinetics and tissue distribution of MTX were compared after intramuscular injection of MTX (treatment I) and MTX-PLL conjugate (treatment II), 10 mg/kg as free MTX to rabbits. The peak concentration of MTX in treatment II were significantly lower than those in treatment I. The amount of MTX excreted in 24-hr urine was significantly reduced in treatment II and it suggested that MTX be more metabolized in treatment II than in treatment I. The amounts of MTX remaining in each organ after 24-hr of intramuscular injection were not significantly different in both treatments.