PubMed Health⌕ Search

Biomedical subjects

J Sudo

Publications and source records attributed to J Sudo.

At least 55 records · Page 3Linked to original sources
PubMed1985

Separation of cephaloridine from the rat urine contaminated by feces and diet pellets in high-performance liquid chromatography. Pretreatment with strongly basic anion exchange resin following deproteinization.

In this study, a high-performance liquid chromatographic method including a treatment with ion exchange resin following a deproteinization treatment, was studied for determination of cephaloridine in the rat urine which was contaminated by pieces of feces and diet pellets. The solvent system used was 10% acetonitrile (v/v) in 0.1 M K2 HPO4-H3 PO4 buffer, pH 7.5, and this was isocratically eluted on a reversed-phase column of NOVA-PAK C18. The urine sample containing cephaloridine was deproteinized, treated with a strongly basic anion exchange resin of Dowex-1-Chloride, and then chromatographed. In comparison to the sample treated by the simple deproteinization, the residual substances after the deproteinization, which interfered the cephaloridine peak, were removed by the following treatment with Dowex-1-Chloride, as was confirmed using a three-dimensional computing spectrophotometric monitor. Thus, the present method is considered to be useful in determination of cephaloridine in such body fluids as urine in which many interfering substances are contained.

Animal Feed↗
PubMed1985

[Study on toxicity of halopredone acetate. (I) Acute toxicity study in mice and rats].

Since halopredone acetate (THS-201), a synthetic corticosteroid, is expected to be used clinically for intra-articular injections because of its long-lasting activity in the synovial bursa, its acute toxicity was compared with that of triamsinolone acetonide (TA) and methylprednisolone acetate (MPA). The test animals were Jcl: ICR mice and Jcl: Wistar rats, and drugs were administered orally, intraperitoneally and subcutaneously. The LD50 values of THS-201 both in mice and rats were estimated more than 5000 mg/kg at each route, and these are for above larger than those of TA or MPA. Moreover, in oral and subcutaneous administration of THS-201, no severe toxic signs were observed either in mice or in rats. In intraperitoneal injection, a few of mice and rats died after showing several clinical signs and suppression of body weight gain, and their autopsy revealed atrophy of thymus, spleen and adrenal, induction of infection and hemorrhage in digestive tract. On the other hand, the mice and rats administered TA or MPA revealed the severe toxic signs such as loss of hair gloss, marked emaciation, decrease in spontaneous movement, anemia, bloated face, decrease or suppression of body weight gain, atrophy of thymus, spleen and adrenal, severe induction of infection and lesions in digestive tracts. Accordingly, it is concluded that the acute toxicity of THS-201 in mice and rats was lower than that of TA or MPA.

Administration, Oral↗
PubMed1985

[Peri- and postnatal study on halopredone acetate in rats].

A peri- and postnatal study of halopredone acetate (THS-201), a synthetic corticosteroid, was carried out using Jcl: Wistar rats. Pregnant rats were treated subcutaneously in doses of 0.05, 0.4, 3.2 and 25.6 mg/kg/day, from day 17 of gestation to day 21 after delivery. All pregnant rats were allowed to litter naturally, and the postnatal development of offsprings was observed. The results obtained from the present study were as follows. No influences of THS-201 administration were observed on gestation, delivery and lactation of dams. THS-201 administration did not have any influences on viability and development, various functions such as reflex response, learning and reproductive performance of F1 generation, and further on development of F2 generation. Therefore, it was concluded that the non-effect dose of THS-201 for the reproduction of dams and development of F1 generation was 25.6 mg/kg/day.

Animals↗
PubMed1985

[Study on toxicity of halopredone acetate. (II). Subacute toxicity study in rats].

Halopredone acetate (THS-201), a synthetic corticosteroid, is expected to be used clinically for intra-articular injection because of its long-lasting activity in the synovial bursa. Subacute toxicity study was carried out on THS-201 by using Jcl: Wistar rats. THS-201 was subcutaneously administered to the rat in doses of 0.1, 0.5, 2.5 and 12.5 mg/kg/day, with the periods for administration and recovery being 3 and 2 months, respectively. Methylprednisolone acetate (MPA) was used for the positive control in dose of 0.5 mg/kg/day. In the group of THS-201 12.5 mg/kg, the below findings were observed: thinning of lumbar hair, swelling of injection site, suppression in body weight gain and decrease of food consumption. The lesions to lymphatic system were indicated by the examinations of peripheral blood, autopsy and histopathology. Slight changes in erythrocytic and biochemical values were seen, and foreign body granuloma was observed in injected subcutis. These findings, exception for lesion of injection site, were almost recovered after the 2 month-recovery period. In the group of THS-201 2.5 mg/kg, some of the changes were noted slightly. In the groups of THS-201 0.5 and 0.1 mg/kg, any toxic changes attributable to THS-201 were not observed. On the other hand, in the group of MPA 0.5 mg/kg, similar findings noted in THS-201 12.5 mg/kg group were observed, but these changes were recovered almost completely at the end of the 2 month-recovery period. It was concluded that the non-toxic dose and the defined toxic dose of THS-201 in this study were 0.5 and 2.5 mg/kg/day, respectively.

Animals↗
PubMed1985

[Study on toxicity of halopredone acetate. (III). Chronic toxicity study in rats].

Chronic toxicity study of halopredone acetate (THS-201), a synthetic corticosteroid, was carried out using Jcl: Wistar rats. THS-201 was subcutaneously administered to the rat in doses of 0.02, 0.1, 0.5 and 2.5 mg/kg/day, with the periods for administration and recovery being 12 and 2 months, respectively. In the group of THS-201 2.5 mg/kg, the below findings were observed: thinning of lumbar hair, suppression in body weight gain, decrease of food consumption in both sexes and decrease of water consumption in male. The lesions to lymphatic system were indicated by the examinations of hemogram, organ weight and histopathology. A few changes in urinary and biochemical values were seen, and foreign body granuloma was observed in the injected subcutis. After 2 month-recovery period, above-mentioned findings almost disappeared. In the group of THS-201 0.5 mg/kg, some of the changes were noted slightly and disappeared after the recovery period. In the groups of THS-201 0.1 and 0.02 mg/kg, any toxic changes attributable to THS-201 were not observed. It was concluded that the non-toxic dose and the defined toxic dose of THS-201 in this study were 0.1 and 0.5 mg/kg/day, respectively.

Animals↗
PubMed1985

[Fertility study on halopredone acetate in rats].

A fertility study of halopredone acetate (THS-201), a synthetic corticosteroid, was carried out using Jcl: Wistar rats. Male rats were treated subcutaneously for 63 days before mating and throughout mating, and female rats were treated subcutaneously for 14 days before mating and until day 7 of gestation, in doses of 0.04, 0.2, 1.0 and 5.0 mg/kg/day. Male and female rats in the same dose were mated. All of the pregnant rats were killed on day 20 of gestation and their fetuses were examined morphologically. The results obtained from the present study were as follows. A decrease in body weight gain was observed in male rats of 1.0 and 5.0 mg/kg groups, compared to the vehicle control group. In female rats of 5.0 mg/kg group, a decrease in body weight gain during gestation period was observed. However, no influences attributable to THS 201 administration were observed on the fertility and fetal development. These results indicated that the non-effect dose of THS-201 for the fertility of rats and fetal development was 5.0 mg/kg/day.

Animals↗
PubMed1985

[Teratogenicity study on halopredone acetate in rats].

A teratogenicity study of halopredone acetate (THS-201), a synthetic corticosteroid, was carried out using Jcl: Wistar rats. Pregnant rats were treated subcutaneously in doses of 0.1, 0.5, 2.5 and 12.5 mg/kg/day, from day 7 to day 17 of gestation. Two-thirds of pregnant rats were killed on day 20 of gestation to examine the development of fetuses, and remaining rats were allowed to litter naturally in order to investigate the postnatal development of offspring. The results obtained from the present study were as follows. During the gestation and lactation periods, there occurred a decrease in the maternal body weight gain in 2.5 and 12.5 mg/kg groups. No influences of THS-201 administration were observed on gestation, delivery and lactation of dams. No external, visceral and skeletal anomalies attributable to THS-201 were observed in the fetuses. THS-201 administration did not have any influences on viability and development, various functions such as reflex response, learning and reproductive performance of F1 generation, and further on development of F2 generation. Therefore, it was concluded that the non-effect dose of THS-201 for the reproduction of dams and development of F1 generation was 12.5 mg/kg/day.

Abnormalities, Drug-Induced↗
PubMed1984

Na+ and K+ cell concentrations in collagenase-treated rat kidney tubules incubated at various temperatures.

Na+ and K+ cell contents were measured in single pieces of tubule (0.4-0.8 mm/sample) micro-dissected from the outer medulla of collagenase-treated rat kidney tissue. Extracellular cations were washed out by rinsing the tubules in ice-cold choline-chloride solution. Na+ and K+ cell contents were measured by emission flame microphotometry after appropriate treatment of the samples. Tubular volumes were calculated from photographic pictures taken before (at 4 degrees C) and after incubation of the samples. Medullary collecting tubules (MCT) and medullary thick ascending limbs of Henle (MAL) were used in this study. When kept at 4 degrees C for 2 h or more, Na+ and K+ concentrations (meq/l cell volume) were 86.3 and 30.6, respectively, in MCT and 16.2 and 94.3, respectively, in MAL. After about 5 min of incubation at 30 degrees C, MCT samples inverted their cation contents up to new steady-state concentrations (Na+ 17.4 and K+ 97.5). During incubation, the volume of MCT samples decreased slowly and in an exponential way, the rate of which was highly temperature dependent. Na+ and K+ cell concentrations in such incubated MCT samples, however, remained fairly constant between 20 and 37 degrees C. In contrast, when MAL samples were incubated at 30 degrees C, Na+ and K+ concentrations (15.9 and 90.4, respectively) remained equal to those measured at 4 degrees C and no change in volume was observed in MAL samples.

Animals↗
PubMed1984

Inhibitory effect of 6-aminonicotinamide on the renal transport of para-aminohippurate in the rat.

In this study, we investigated the effect of 6-aminonicotinamide (6-AN), a typical potent inhibitor of the pentose phosphate pathway, on the renal transport of para-aminohippurate (PAH) in the rat. The contents of adenosine-triphosphate (ATP) and 6-phosphogluconate (6-PG) in the kidney were measured at intervals of 2 hours after the administration of 6-AN (75 mg/kg body weight, i.p.). It was found that the 6-PG content in the kidney rapidly increased and reached a plateau at the fourth hour after the administration, with this level being maintained up to the eighth hour. In contrast, the ATP content was found to remain normal up to the sixth hour, after which it significantly decreased as time elapsed. Furthermore, additional experiments were carried out by loading the rat with a high concentration of PAH solution at 6 hours after the administration of 6-AN. The renal tubular secretion maximum for PAH was significantly depressed in the 6-AN group in comparison to the control. These results suggest that this depression in renal PAH secretion capacity was partially due to the inhibition of the pentose phosphate pathway in the kidney, but not due to the change of renal ATP level.

6-Aminonicotinamide↗
PubMed1984

Inhibitory effect of nicotine on chemiluminescence response of human polymorphonuclear leukocytes stimulated by opsonized zymosan in vitro.

Effect of nicotine on chemiluminescence (CL) responses of human polymorphonuclear leukocytes (PMN) in vitro was investigated. Nicotine, ranging from 10(-5) to 5 X 10(-4)M, showed a concentration-dependent inhibition of the CL induced by 2.5 mg of opsonized zymosan. This inhibitory effect of nicotine (10(-4)M) on CL was not affected by atropine (10(-4)M), hexamethonium (10(-4)M) or acetyl beta-methylcholine (10(-4)M). These results indicate that nicotine directly acts to PMN with no relation of cholinergic affecting receptors. As to cytotoxic effects on PMN, assessed by the methods of trypan blue exclusion and of lactate dehydrogenase leakage from the cells, nicotine showed no cytotoxic effect on PMN in its range of 10(-5) to 5 X 10(-4)M. It is concluded that tobacco alkaloid nicotine could directly inhibit phagocytizing function of PMN. Furthermore, it is presumed that PMN circulating in the respiratory organs in tobacco smoking would be exposed to high concentrations of nicotine, and that the nicotine incorporated into the circulating system could suppress PMN functions resulting in harmful influences on the host defense mechanisms.

Cells, Cultured↗
PubMed1984

Allopurinol toxicity: its toxic organ-specificity between the liver and the kidney in the rat.

In this study, allopurinol toxicity was investigated in the liver and the kidney in the rat. Allopurinol was intraperitoneally administered to rats, once a day, for 1, 3 or 10 days, in doses of 3, 10, 30 and 100 mg/kg body weight/day. At the 24th hour after the last administration, the rat was sacrificed, and blood and tissue samples were taken for analyses. In doses of 30 mg/kg/day and more, decreases of the body weight and the liver weight were observed, while the kidney weight increased. The plasma activities of alkaline phosphatase, glutamic oxaloacetic and glutamic pyruvic transaminases showed no increases, while the blood urea nitrogen and creatinine increased. These changes were the most remarkable in the 3 day administration, whereas they approached the control level thereafter. In doses of 10 mg/kg/day and less, no significant changes were observed in comparison to the control. These results denote that the minimal toxic dose ranges between 10 and 30 mg/kg/day, and that the kidney is more sensitive than the liver. In addition, these results also denote that the renal and hepatic failures are reversively restored even when allopurinol is further administered later than the 3 day. This fact suggests not only that the capacity inactivating allopurinol in the body is increased, but also that the enzymatic induction in the allopurinol inactivation system is accelerated.

Allopurinol↗
PubMed1984

Inhibition of glucose reabsorption induced by 6-aminonicotinamide in the rat kidney.

The relationship between natriuresis and glucosuria produced by administration of 6-aminonicotinamide (6-AN), was investigated in the rat. After intraperitoneal administration of 6-AN (75 mg/kg), urine was collected at intervals of 2 hours using a metabolic cage for assays. Sodium and glucose were excreted maximally into the urine at 2 to 4 and at 4 to 6 hours, respectively, after the administration of 6-AN, with a time delay being recognized between sodium and glucose in the peaks of their urinary excretions. This dissociation of the patterns on the urinary excretion between sodium and glucose led to the following conclusion that the natridiuresis induced by 6-AN was not mainly ascribed to the osmotic diuresis for glucose, but to the direct effect on the sodium transport in the kidney. Furthermore, additional experiments were carried out by loading animals with glucose after administration of 6-AN. The tolerance for glucose in the body was clearly depressed in rats in the 6-AN group, while no significant difference in the renal threshold concentration for glucose was shown in either group. The renal tubular transport maximum for glucose was also depressed in the 6-AN group. It is, accordingly, speculated that the glucosuria induced by 6-AN was not only due to the hyperglycemia, but also due to the decreased capacity of the renal tubular reabsorption for glucose.

6-Aminonicotinamide↗
PubMed1982

Urinary prostaglandins and kallikrein in the course of acute renal failure.

To examine the role of prostaglandins and the kallikrein system in the recovery from acute renal failure, we studied the sequential changes in urinary prostaglandins and kallikrein after the onset of oliguria. The six patients studied had acute tubular necrosis of the vasomotor type. Urinary PGE2, PGF2 alpha, the PGF2 alpha-main urinary metabolite, 6-keto-PGF1 alpha and TXB2 were all measured by radioimmunoassay. Urinary kallikrein was assayed by means of hydrolytic activity using a chromogenic tripeptide substrate. Following onset of diuresis, urinary PGE2 excretion was increased to normal, parallel to the increase in urine volume. In contrast, the ratio of urinary PGF2 alpha/PGE2 peaked at the onset of diuresis, indicating a relative increase in PGF2 alpha production at this time. Prior to this peak, urinary kallikrein concentrations reached the highest levels, suggesting a close connection with renal prostaglandin metabolism. On the other hand, changes in PGF2 alpha-MUM, 6-keto-PGF1 alpha and TXB2 were not found. These results indicate that there may be an interlocking acute alteration of the kallikrein-prostaglandin system occurring immediately before the resolution of oliguria, although the role of the acute shift to PGF2 alpha production observed needs further study.

Acute Kidney Injury↗