Biomedical subjects

S Kojima

Publications and source records attributed to S Kojima.

At least 703 records · Page 39Linked to original sources

PubMed1990

Effect of N-benzyl-D-glucamine dithiocarbamate on renal toxicity induced by cadmium-metallothionein in rats.

The effect of N-benzyl-D-glucamine dithiocarbamate (BGD) on the renal toxicity induced by acute exposure to cadmium-metallothionein (Cd-MT) in rats was studied. Rats were injected intraperitoneally with BGD (400 mumol/kg) 6, 12, or 24 h after intraperitoneal injection of Cd-MT (1.78 mumol Cd as Cd-MT/kg) and thereafter they received three injections of BGD (400 mumol/kg) daily for 3 days. Urinary protein concentration and aspartate aminotransferase (AST) activity significantly increased 1 day after Cd-MT treatment and decreased to control levels at 9 days after the treatment. Urinary excretion of glucose and amino acids rose gradually reaching maximum levels 5 days after Cd-MT treatment and returned to the control levels at 9 days. BGD injection significantly reduced the increases in the urinary excretion of protein, AST, glucose and amino acid, which were produced by Cd-MT treatment. Significant increases in urine volume were observed after Cd-MT treatment. BGD injection inhibited the increase in urine volume caused by Cd-MT treatment. A long time interval (12 and 24 h) between the administrations of Cd-MT and BGD resulted in a decreased protective effect of BGD against Cd-MT-induced renal damage. Following Cd-MT injection, the major route of excretion of cadmium (Cd) was via the urine and the kidney was the major site of accumulation of Cd. BGD injection remarkably increased the urinary excretion of Cd, resulting in a significant reduction in the kidney Cd concentration. The results of this study indicate that BGD injection is effective in decreasing the Cd concentration in the kidney, resulting in the protective effect on Cd-MT-induced renal damage.

Amino Acids↗

PubMed1990

Angiostrongylus cantonensis: in vitro cultivation from the first-stage to infective third-stage larvae.

The first-stage larvae of Angiostrongylus cantonensis were cultured in various media at 27 degrees C. The most suitable medium for the development was Chernin's balanced salt solution supplemented with 10% L-15, 10% tryptose phosphate broth, 20% fetal calf serum, and 26 mM sodium bicarbonate. Addition of sodium bicarbonate to the medium facilitated early development of the first-stage larvae. When the first-stage larvae were cultured in the medium under 5% CO2 in air, the worms developed gradually to become quiescent and showed the C shape. Thereafter, the larvae developed to the second stage, retaining their first sheath. About 23 days later, the larvae began to develop to the third stage, being enclosed within the sheaths of the first and second molts. Under these conditions, the larvae developed uniformly and 82% of the larvae reached the third stage 50 days later. About 70% of the third-stage larvae discarded their two sheaths, showing almost the same size as those obtained in vivo. When these exsheathed larvae were inoculated into rats, they developed into adult worms and deposited numerous first-stage larvae.

Angiostrongylus↗

PubMed1990

Possible role of renal prostaglandin E2 in natriuresis associated with supraventricular tachycardia.

We investigated the possible role of renal prostaglandin (PG) E2 in natriuresis associated with supraventricular tachycardia (SVT). In five female patients with paroxysmal tachycardia, SVT was artificially induced and then stopped 60 min later. Before, during, and after SVT, plasma levels of arginine vasopressin and atrial natriuretic peptide (ANP) and the urinary excretion of sodium and PGE2 were measured. Polyuria was observed during SVT. However, natriuresis did not occur until immediately after the termination of SVT. During SVT, the plasma levels of arginine vasopressin tended to decrease. When SVT was terminated, the vasopressin levels increased significantly (p less than 0.01). Urinary excretion of PGE2 tended to decrease during SVT and then increased significantly (p less than 0.01) after SVT ended. Urinary excretion of sodium was correlated (r = 0.699, p less than 0.001) with the urinary excretion of PGE2. Plasma ANP increased during SVT, but there was no correlation with urinary sodium excretion. These results suggest that renal PGE2, the biosynthesis of which may be stimulated by a increase in plasma vasopressin, is an important factor contributing to the natriuresis observed after the end of SVT.

Adult↗

PubMed1990

Genuine CD7 expression in acute leukemia and lymphoblastic lymphoma.

CD7 has been used as a valuable marker for normal and malignant T cells and also for a proportion of acute nonlymphocytic leukemia (ANLL) cells. Difference in reactivity was noticed among CD7 antibodies, however, when tested against ANLL cells and myeloid/monocytoid cell lines; Tp40 antibody produced in our laboratories was not reactive with the HL-60 promyelocytic line, whereas 4A antibody was reactive, even though both detected a quite similar or an identical epitope on CD7 molecule. Preincubation of HL-60 cells with human immunoglobulin preparation clearly negated the reactivity by 4A, suggesting that 4A antibody is not reactive to CD7 itself, but it probably binds with immunoglobulin G Fc receptors expressed on HL-60 cells. Five cases of ANLL which were positive with 4A antibody were selected and tested with Tp40 antibody, and only two were found to be positive. Expression of CD7 mRNA in these two cases (but not in other cases) was also demonstrated by Northern blotting with a cDNA probe for CD7 recently cloned in our laboratories, indicating that CD7 is expressed on a certain fraction of ANLL, although the positive cases may be smaller than the reports so far appeared. A Northern blot study was also conducted with two acute lymphocytic leukemia cases and one lymphoblastic lymphoma case with CD7+, CD2-/+/-, CD5-/+/- phenotype and germline T cell receptor beta genes. CD7 mRNA is expressed in all three cases and CD3 mRNA is also observed in two cases, suggesting that these tumor cells are of T precursor origin.

Acute Disease↗

PubMed1990

Alteration of the specificity of the Streptomyces subtilisin inhibitor by gene engineering.

We have altered the amino acid at the center of the reactive site (methionine 73) of Streptomyces subtilisin inhibitor (SSI) by site-directed and cassette mutagenesis. Replacement by lysine or arginine resulted in trypsin inhibitory activity, replacement only by lysine gave inhibition of lysyl endopeptidase, and replacement by tyrosine or tryptophan resulted in inhibition of alpha-chymotrypsin. The four mutant SSIs retained their native activity against subtilisin BPN'. Thus by altering only one amino acid residue at the reactive site of SSI to the substrate specificity of the respective protease we could successfully change its inhibitory profile.

Amino Acid Sequence↗

PubMed1990

Sodium sensitive and sodium retaining hypertension.

The differences between sodium sensitive and sodium retaining hypertension were theoretically considered using a water tank model of body fluid volume-blood pressure regulation. If an outlet valve is attached to a tank with a base area corresponding to the reciprocal of total peripheral resistance (TPR) and water is poured into this tank at a rate corresponding to the amount of Na+ intake, then equilibrium should be achieved at a certain water level, volume and output from the outlet, which represent mean arterial pressure (MAP), cardiac output (CO) and urinary Na+ excretion. The height of the outlet from the tank bottom and the size cross-sectional area, of the outlet correspond to the x-intercept and slope of the renal function (pressure-natriuresis) curve, respectively. In both nonsodium sensitive hypertension, due to the shift of the curve toward a higher blood pressure level (elevated height of the outlet) without change in the slope (size of the outlet), and sodium sensitive hypertension, due to the depressed slope of the curve (reduced outlet size), not only MAP (water level) but also CO (water volume) are increased, resulting in sodium retaining hypertension, if TPR (reciprocal of base area) remained unchanged, while CO is relatively unchanged, resulting in nonsodium retaining hypertension, if TPR is elevated. Thus, the MAP and its sensitivity to sodium intake is determined by the renal function curve. Since body fluid volume is determined by both the renal function curve and TPR, however, changes in TPR during the development of hypertension is a major factor in determining whether or not the body fluid volume has to change only a small amount or a large amount. Therefore, the sodium sensitivity of blood pressure and sodium retention must be considered separately.

Blood Pressure↗

PubMed1990

Normalization of increased sodium sensitivity by maintenance hemodialysis.

Blood pressure (BP) becomes more sodium and body fluid sensitive as renal function deteriorates. Thus, hypertension in chronic renal failure is mostly of the sodium sensitive type. We studied whether the increased sodium sensitivity (SS) can be restored to normal on the maintenance phase of hemodialysis (HD) therapy. Body weight (BW) and BP (specifically, mean arterial pressure [MAP]) were measured after HD and before the next HD, and the body fluid sensitivity (BFS) was calculated as the ratio of changes in these factors on both introduction and maintenance phases in HD patients (n = 56) who were not taking any antihypertensive drugs (BFS = delta MAP/delta BW). In a preliminary study, the amount of interdialytic sodium intake (QNa+) was measured (n = 30), and SS was calculated as the ratio of the change in MAP to QNa+ (SS = delta MAP/QNa+). Interdialytic BW gain (3.1 +/- 0.1 kg) was correlated with the amount of sodium intake (136 +/- 17 mEq), resulting in a positive relationship between BFS and SS (r = 0.79, P less than .0001). Therefore, BFS was used as an index of SS. As a whole, BFS decreased from the introduction to the maintenance phase (6.5 +/- 1.0 to 3.5 +/- 0.6 mm Hg/L, P less than .01). This decrease was marked (6.2 +/- 1.1 to 2.9 +/- 0.6 mm Hg/L, P less than .01) in patients (n = 46) whose BP was normalized in the maintenance phase, while not significant (7.9 +/- 1.9 to 6.3 +/- 1.3 mm Hg/L) in patients (n = 10) whose BP was still high.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

Determination of effective and safe dose for intracoronary administration of nicorandil in dogs.

STUDY OBJECTIVE: The aim was to evaluate the effective and safe dosage for intracoronary administration of nicorandil (2-nicotinamidoethyl nitrate) in dogs. DESIGN: Five ml of saline with or without nicorandil (0.025, 0.25, 1.0 or 2.5 mg) was constantly infused into the left anterior descending coronary artery (LAD) in 1 min without blood flow reduction in group A (normoxic group, n = 5) and with 50% blood flow reduction of the control value in group B (ischaemic group, n = 5). SUBJECTS: 10 mongrel dogs of either sex were used, weight 14.6-20.5 kg. MEASUREMENTS AND MAIN RESULTS: The myocardial weight of the perfused area was 33.2(SD 7.9) g. In group A, LAD blood flow increased from 28.4(8.6) to 86.3(25.0) ml.min-1, p less than 0.05, following intracoronary infusion of 0.25 mg nicorandil. Higher doses caused no further increase. In both groups, high doses (1.0 mg or more) suppressed regional myocardial contraction, expressed as % segment shortening, from 20.0(4.7) to 10.0(9.0)%, p less than 0.05, in group A, and from 12.7(8.5) to 6.5(5.6)%, p less than 0.05, in group B. Multiple ventricular premature beats developed in both groups only at the dose of 2.5 mg: 6.8(5.5) beats.min-1 in group A and 4.5(4.2) beats.min-1 in group B. Ventricular fibrillation developed in two dogs in group B. Nicorandil did not affect the local bipolar electrocardiogram of the subendo- and subepicardium in the perfused area in either group. CONCLUSIONS: Intracoronary administration of 0.25 mg of nicorandil was effective for coronary vasodilatation without deleterious mechanical or electrical effects. Larger doses of the agent showed adverse effects depending on the dosages.

Animals↗

PubMed1990

Effect of inhibitory activity of mutation at reaction site P4 of the Streptomyces subtilisin inhibitor, SSI.

The protein Streptomyces subtilisin inhibitor, SSI, efficiently inhibits a bacterial serine protease, subtilisin BPN'. We recently demonstrated that functional change in SSI was possible simply by replacing the amino acid residue at the reactive P1 site (methionine 73) of SSI. The present paper reports the additional effect of replacing methionine 70 at the P4 site of SSI (Lys73) on inhibitory activity toward two types of serine proteases, trypsin (or lysyl endopeptidase) and subtilisin BPN'. Conversion of methionine 70 at the P4 site of SSI(Lys73) to glycine or alanine resulted in increased inhibitory activity toward trypsin and lysyl endopeptidase, while replacement with phenylalanine weakened the inhibitory activity toward trypsin. This suggests that steric hindrance at the P4 site of SSI(Lys73) is an obstacle for its binding with trypsin. In contrast, the same P4 replacements had hardly any effect on inhibitory activity toward subtilisin BPN'. Thus the subsite structure of subtilisin BPN' is tolerant to these replacements. This contrast in the effect of P4 substitution might be due to the differences in the S4 subsite structures between the trypsin-like and the subtilisin-like proteases. These findings demonstrate the importance of considering structural complementarity, not only at the main reactive site but also at subsites of a protease, when designing stronger inhibitors.

Bacterial Proteins↗

PubMed1990

Phosgene (chlorophenyl)hydrazones, strong sensitizers found in yellow sweaters bleached with sodium hypochlorite, defined as causative allergens for contact dermatitis by an experimental screening method in animals.

12 young men developed allergic contact dermatitis from wearing yellow cotton sweaters. We attempted to identify the causative agents by an experimental screening method in animals. Guinea pigs were sensitized with an acetone extract of the sweater material, by means of the guinea pig maximization test (GPMT). Active ingredients were then separated from the extract, by step-by-step patch test screening of chromatographic fractions in the guinea pigs, and finally analyzed by gas chromatography-mass spectrometry (GC-MS). Although there were 2 allergens with important activity (1 in the fraction eluted from the silica gel column with hexane, and 1 in the methanol fraction), the present study is focussed on the fat-soluble allergens in the hexane fraction. GC-MS analysis revealed that 4 kinds of phosgene (chlorophenyl)hydrazones (PCPHs) were present in the hexane fraction. PCPHs prepared in our laboratory showed strong eliciting activities, not only in the guinea pigs sensitized with the extract, but also in a male volunteer sensitized by exposure to a yellow sweater during irritancy testing. Phosgene (2,5-dichlorophenyl)hydrazone, which was the main component among the PCPHs found in the sweater, sensitized guinea pigs even at the 1 ppm level. From these results, we conclude that PCPHs were one of the allergens responsible for the cases.

Animals↗

PubMed1990

Inhibitory effect of renal nerve activity during canine anaphylactic hypotension.

We have examined baroreceptor regulation of renal nerve activity (RNA) during anaphylactic hypotension that affects renal nerve activity. In anesthetized dogs, mean blood pressure (MBP), heart rate (HR), and RNA were simultaneously measured. To test for a normally functioning baroreceptor reflex in each animal, a transient hypotension was induced by an intravenous injection of sodium nitroprusside (4 micrograms/kg). Nitroprusside produced a reflex increase in RNA (+63 +/- 12% at -20 mmHg and +139 +/- 8% at -40 mmHg) and HR (+13 +/- 1 beats/min at -20 mmHg and +21 +/- 2 beats/min at -40 mmHg). However, intravenous administration of Ascaris suum antigen in animals with an intact neuraxis caused a decrease in RNA (-15 +/- 14% at -20 mmHg and -42 +/- 11% at -40 mmHg blood pressure during the antigen-induced hypotension) in parallel with a fall in systemic blood pressure. HR responses were -5 +/- 2 beats/min at -20 mmHg and -10 +/- 1 beats/min at -40 mmHg during the hypotension induced by the antigen. In animals with combined denervation of the carotid sinus and vagal nerves, HR did not change significantly during anaphylactic hypotension. However, a decrease in RNA remained (-60 +/- 4% at -20 mmHg and -72 +/- 4% at -40 mmHg of hypotension). The decrease in RNA after antigen administration was significantly greater after denervation than in animals with an intact neuraxis. These results indicate that systemic baroreceptor reflex control of RNA is reduced during anaphylactic hypotension. Impaired reflex control of sympathetic nerve activity may result from an impairment of sympathetic outflow through the central nervous system.

Anaphylaxis↗

PubMed1990

Comparison of auditory functions in the chimpanzee and human.

Absolute thresholds for pure tones, loudness, frequency and intensity difference thresholds and the resonance of the external auditory meatus were measured in chimpanzees and compared with those in humans. Chimpanzees were more sensitive than humans to frequencies higher than 8 kHz but less sensitive to frequencies lower than 250 Hz and 2- to 4-kHz tones. Difference thresholds for frequency and intensity were greater in chimpanzees than in humans. The resonance of the external ear was about the same in the two species. The effects of differences in hearing between species upon speech perception are discussed.

Adult↗

PubMed1990

Prognosis and disability of stroke patients after 5 years in Akita, Japan.

The system of registering stroke patients was begun in 1963 in Ikawa Town, Akita Prefecture, Japan. The town is located in the northeastern part of the country and in 1975 had a population of 6,427. From 1975 to 1981, 109 patients who suffered their first stroke were registered and were monitored for 5 years. The average annual incidence rates of stroke were 2.8 and 2.0 per 1,000 population in males and females, respectively. Mean age at stroke onset was 63.3 and 71.4 years in males and females, respectively (p less than 0.01). According to the clinical classification of stroke, 76 patients suffered cerebral infarction, 21 cerebral bleeding, and six subarachnoid hemorrhage; six strokes were unclassified. The survival rates were compared by sex, age, and clinical stroke type using Cox's proportional hazards model. The survival rate of female stroke patients was lower than that of males, but not significantly so. The survival rate of stroke patients greater than or equal to 65 years old was significantly lower (p less than 0.01) than that of younger patients. Moreover, the survival rate of patients with cerebral bleeding was significantly lower (p less than 0.01) than that of patients with cerebral infarction. In the analysis of self-care among the survivors, performance of the activities of daily living in older patients indicated significantly less independence (p less than 0.01) in younger patients. Follow-up of new stroke cases showed that age and clinical stroke type were significantly associated with survival and that age was also related to disability of the survivors.

Activities of Daily Living↗

PubMed1990

Effect of N-benzyl-D-glucamine dithiocarbamate on renal toxicity of inorganic mercury in rats.

The effect of N-benzyl-D-glucamine dithiocarbamate (BGD) on the renal toxicity of inorganic mercury in rats was studied. Rats were injected i.v. with saline or HgCl2 (300 micrograms Hg/kg) and 30 min later they were injected i.p. with saline or BGD (2778 mumol/kg, a quarter of an LD50). Urinary excretion of gamma-glutamyl-transpeptidase (gamma-GTP), which is a brush border enzyme, in rats after mercury treatment significantly increased compared to that of the control in the 12-24 h urine specimen and reached a maximum value within 24 h after the treatment. Urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG), which is a lysosomal enzyme, also significantly increased after mercury treatment compared to that of the control in the 12-24 h urine specimen and reached a maximum value within 48 h after the treatment. A change in urinary aspartate aminotransferase (AST) activity after mercury treatment followed a pattern similar to that observed with the urinary NAG. BGD treatment did not increase the urinary excretions of gamma-GTP, NAG, and AST. The uptake of p-aminohippuric acid (PAH) by renal cortical slices significantly decreased 24 h after mercury treatment. BGD injection after mercury treatment did not decrease the uptake of PAH by cortical slices. In addition, the microscopic examination of renal tissue from mercury-treated rats revealed necrosis of the proximal tubular cells. However, a photomicrograph of rat renal cortex after BGD treatment showed little abnormality. These results indicated that the mercury-induced renal damage was protected by the injection of BGD 30 min after mercury treatment.

Animals↗

PubMed1990

Protective effect of N-benzyl-D-glucamine dithiocarbamate against cis-diamminedichloroplatinum-induced toxicity in gastrointestinal tract and bone marrow in rats.

The protective effect of N-benzyl-D-glucamine dithiocarbamate (BGD) against gastrointestinal and bone marrow toxicities produced by cis-diamminedichloroplatinum (DDP) injection in rats was studied. Rats were injected i.p. with BGD (2 mmol/kg) immediately after i.v. injection of DDP (20 mumol/kg). A scanning electron micrograph of the jejunum after DDP treatment showed damage in the villi, and that BGD protected the DDP-induced jejunal damage. BGD treatment also had a protective effect against DDP-induced diarrhea. BGD significantly reversed the reduction in maltase and sucrase activities of jejunal mucosa of rats treated with DDP. Platinum (Pt) concentrations in the gastrointestine as well as in the kidney and liver after DDP injection decreased following BGD treatment. The reduction of leukocytes following DDP injection returned to control values after BGD treatment. Biliary and urinary excretions of Pt after DDP injection was remarkably increased by BGD treatment. The results of this study indicated that the injection of BGD to rats treated with DDP can effectively remove Pt from the body through biliary and urinary excretions, resulting in protection of the gastrointestinal and bone marrow toxicities induced by DDP treatment.

Animals↗

PubMed1990

Alkylnaphthalene. XI. Pulmonary toxicity of naphthalene, 2-methylnaphthalene, and isopropylnaphthalenes in mice.

Pulmonary toxicity of naphthalene (NAP), 2-methylnaphthalene (2-MN), 2-isopropylnaphthalene (2-IPN) and 2,6-diisopropylnaphthalene (2,6-DIPN) was studied in mice. Twenty four h after the intraperitoneal (i.p.) administration of NAP (200 mg/kg (1.6 mmol] or 2-MN (400 mg/kg (2.8 mmol], pulmonary damage was detected. Prior treatment with diethyl maleate resulted in enhancement of NAP and 2-MN-induced bronchiolar damage. In contrast to the effects of NAP and 2-MN, injections of 2-IPN (3000 mg (17.6 mmol)/kg) and 2,6-DIPN (3000 mg (14.2 mmol)/kg) did not cause detectable pulmonary damage. Injections of NAP and 2-MN caused considerable depletion of pulmonary reduced glutathione (GSH), while injections of 2-IPN and 2,6-DIPN caused only a slight depletion. There were general decreases in the binding of the compounds to lung slices with increasing number of carbons of the alkyl substituent. Pretreatment with a cytochrome P-450 inducer (beta-naphthoflavone) increased the binding of NAP, 2-MN, and 2-IPN to lung slices. Treatments with NAP, 2-MN, 2-IPN and 2,6-DIPN did not affect the lipid peroxidation or phospholipid contents in the lung. These results suggest that the difference in pulmonary toxicity among NAP, 2-MN, 2-IPN, and 2,6-DIPN may be dependent on the ability of these compounds to irreversibly bind to lung tissue.

Animals↗

PubMed1990

Effects of three dithiocarbamates on tissue distribution and excretion of cadmium in mice.

N-Benzyl-D-glucamine dithiocarbamate (BGD), N-p-hydroxymethylbenzyl-D-glucamine dithiocarbamate (HBGD), and N-p-carboxybenzyl-D-glucamine dithiocarbamate (CBGD) were compared for their relative efficacies in the distribution and excretion of cadmium in mice exposed to cadmium. Mice were injected intraperitoneally with 109CdCl2 (1 mg of Cd/kg and 2 microCi of 109Cd/one animal). Three days later, they were injected with chelating agents (400 mumol/kg) every other day for 2 weeks. After injections of BGD and HBGD, cadmium was excreted mainly in the feces through the bile, and the fecal excretion of cadmium by HBGD was significantly higher than that by BGD or CBGD. These chelating agents increased the urinary excretion of cadmium to a small extent. The hepatic cadmium content was decreased only after HBGD injection. Also, the injection of HBGD caused a much greater decrease in renal cadmium content than did BGD or CBGD. These chelating agents did not result in the redistribution of cadmium to the brain, testes, or heart. The growth of mice was only slightly retarded by injections of these chelating agents. The results of this study indicate that the injection of HBGD to mice pretreated with cadmium can remove cadmium from the body, mainly through fecal excretion, without redistribution of cadmium to other tissues such as the brain, testes, and heart, more effectively than BGD or CBGD.

Animals↗

PubMed1990

Effects of several dithiocarbamates on tissue distribution and excretion of inorganic mercury in rats.

The effects of various chelating agents, sodium N-benzyl-D-glucamine dithiocarbamate (BGD), sodium N-p-methylbenzyl-D-glucamine dithiocarbamate (MBGD), sodium N-p-hydroxymethylbenzyl-D-glucamine dithiocarbamate (HBGD), and N-p-carboxybenzyl-D-glucamine dithiocarbamate (CBGD), which were newly synthesized, and sodium N-methyl-D-glucamine dithiocarbamate (MGD), on the distribution and excretion of inorganic mercury were compared in rats exposed to HgCl2. Rats were injected i.p. with 203HgCl2 (300 micrograms of Hg and 74 kBq of 203Hg/kg) and 30 min or 24 h later, they were injected with a dithiocarbamate (1200 mumol/kg). At 30 min after mercury administration, BGD and MBGD significantly enhanced the biliary excretion of mercury, while CBGD, MGD, and HBGD enhanced the urinary excretion of mercury to a small extent. At 24 h after mercury injection, BGD was the most effective on the biliary excretion of the metal, while MGD and HBGD significantly enhanced the urinary excretion of the metal. All of these dithiocarbamates were effective in mobilizing mercury from the kidney at 30 min after mercury treatment. At 24 h after mercury treatment, HBGD and BGD effectively depressed mercury content in the kidney. These results show that the injection of BGD and HBGD at both 30 min and 24 h after mercury treatment can much more effectively mobilize mercury from the kidney without redistribution of mercury to other tissues, such as brain, heart, and lung, when compared with injection of other chelating agents. The pattern of mobilization and excretion of mercury following treatment with each chelating agent was related to the organic/aqueous partition coefficient of each dithiocarbamate-mercury complex.

Animals↗