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Biomedical subjects

Y Suketa

Publications and source records attributed to Y Suketa.

At least 19 recordsLinked to original sources
PubMed1992

Effect of nitrite on cell growth and antibody production in mouse splenic B cells stimulated with lipopolysaccharide and B cell hybridomas.

Nitric oxide, nitrite and nitrate are released by activated macrophages in an immune response. We showed here that nitrite influenced cell growth and antibody production in mouse lipopolysaccharide (LPS)-stimulated splenic B cells and B cell hybridomas. The addition of 10(-7) and 10(-6) M nitrite enhanced deoxyribonucleic acid (DNA) synthesis of LPS-stimulated splenic B cells. However, DNA synthesis and antibody production in the case of total spleen cells stimulated with LPS were suppressed by nitrite in a dose dependent-manner. These phenomena were also observed in a similar experiment involving mouse B cell hybridomas. Antibody production of all B cell hybridomas was significantly suppressed by the addition of nitrite. This suppressing effect could not be explained by changes in viable cell yields. This data suggests that the antibody production and cell proliferation of B cells may be influenced by nitrite from activated macrophages in the immune response.

Animals↗
PubMed1991

cAMP activates Cl-/HCO-3 exchange for regulation of intracellular pH in renal epithelial cells.

The role of cAMP in regulation of intracellular pH in the confluent LLC-PK1 cells was investigated. DibutyrylcAMP and forskolin induce intracellular acidification. This acidification is inhibited by DIDS and ethacrynic acid, inhibitors of Na(+)-independent Cl-/HCO3- exchange, and by removal of extracellular Cl-. In addition, Bt2 cAMP causes Cl- entry into LLC-PK1 cells. These results suggest that cAMP activates Cl- transport, namely Na(+)-independent Cl-/HCO3- exchange, which participates in pHi regulation.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1991

Induction of nitrite production in mouse spleen cells by immunization.

Changes of nitrite production in mouse spleen cells of in vitro secondary antibody response were investigated. Mouse spleen cells immunized with gamma globulin fraction of rat serum produced nitrite 3 days after in vitro challenging with the same antigen. Nitrite production of rabbit IgG-challenged spleen cells was found to be about 2.9-times higher than that of spleen cells primed with the gamma globulin fraction of rat serum. Nitrite production in this system was completely suppressed by T cell depletion (99.7% inhibition). Furthermore, nitrite production in these cells significantly decreased by addition of anti-interferon gamma antibody (62.9% inhibition). These data indicate that nitrite production in antigen-immunized spleen cells is affected with the immunogenicity of an antigen and regulated by T cells, especially interferon (IFN) gamma.

Animals↗
PubMed1991

Effect of recombinant human interleukin-6 on nitrite production of mouse myeloid leukemia cells.

The effect of recombinant human interleukin-6 (rhIL-6) on induction of nitrite (NO(-2)) production was investigated in a mouse myeloid leukemia cell line (M1) and a subclone (Mm1). NO(-2) was induced by rhIL-6 (greater than 50 U/ml) in these cell lines. Pretreatment with rhIL-6 (100 U/ml) for 1 day synergistically enhanced the production of NO(-2) in Mm1 by LPS. Furthermore, pretreatment with IL-6 (100 U/ml) shortened the lag time of induction. These results indicate that IL-6 is involved in the regulation of the NO(-2) production in macrophage-like cells.

Animals↗
PubMed1990

Effects of Ca2+, Zn2+ and Cd2+ on uridine diphosphate-glucuronyltransferase and beta-glucuronidase activities in rat liver microsomes.

The effect of various metals on uridine diphosphate (UDP)-glucuronyltransferase and beta-glucuronidase activities in rat liver microsomes was investigated. The presence of Mn2+, Cd2+, Zn2+, V5+, Ni2+, Co2+, Cu+ or Ca2+ (20 microM) in the enzyme reaction mixture did not cause a significant alteration of UDP-glucuronyltransferase activity in hepatic microsomes. Of these metals, Zn2+ and Cd2+ (20 microM) caused a remarkable increase in hepatic microsomal beta-glucuronidase activity. Appreciable effects of Zn2+ and Cd2+ on beta-glucuronidase activity were seen at 5.0 microM, and the effects were saturated at 50 microM. Ca2+ (5.0-50 microM) and/or the Ca2(+)-binding protein regucalcin (2.0 microM) did not have an appreciable effect on UDP-glucuronyltransferase and beta-glucuronidase activities in hepatic microsomes. Thus, Zn2+ and Cd2+ uniquely increased beta-glucuronidase activity. The Zn2(+)- and Cd2(+)-induced increase in beta-glucuronidase activity was completely reversed by the presence of an SH group-protecting reagent (dithiothreitol). The response of the microsomal enzyme to Zn2+ and Cd2+ (20 microM) was no longer seen after treatment with 0.2% Triton X-100 [polyoxyethylene(10)octylphenyl ether], indicating that the stimulation by these metals is dependent on membrane association. The present study suggests that, of various metals tested, Zn2+ and Cd2+ can uniquely increase hepatic microsomal beta-glucuronidase activity and that their effect is based on binding to membranous SH groups, beside the enzyme protein.

Animals↗
PubMed1990

Alteration of glucose consumption and adenosine triphosphate content in bone tissue of rats with different ages: the stimulatory effect of zinc.

The alteration in bone metabolism at different ages was investigated by estimating glucose consumption and adenosine triphosphate (ATP) content in a culture system of bone tissue from 3- and 30-week-old rats. The femoral-diaphyseal tissue was removed and cultured for periods up to 48 h in Dulbecco's Modified Eagle Medium. Bone tissue was incubated at 37 degrees C in 5% CO2/95% air in a medium containing either vehicle and zinc sulfate (10(-6) - 10(-4) M). The medium glucose consumed by bone tissue clearly increased in a 48 h-culture in 3-week-old rats, while the increase in 30-week-old rats was slight. The presence of zinc sulfate (10(-6) and 10(-5) M) caused a significant increase in bone glucose consumption in 3- and 30-week-old rats. ATP content in cultured bone tissue from 30-week-old rats fairly fell in comparison with that from 3-week-old rats. Bone ATP contents in 3- and 30-week-old rats were significantly increased by the presence of zinc (10(-4) M). The present findings suggest that bone energy metabolism deteriorates with increasing age, and that zinc has a stimulatory effect in elderly rats.

Adenosine Triphosphate↗
PubMed1989

Effect of vanadium on bone metabolism in weanling rats: zinc prevents the toxic effect of vanadium.

The effect of vanadium on bone metabolism was investigated in the femoral diaphysis of weanling rats. Vanadium pentoxide (1.0-20.0 mumol V/100 g b.wt.) was administered orally for 3 days. The doses of 15.0 and 20.0 mumol V/100 g caused a significant increase in serum calcium concentration. Bone alkaline phosphatase activity was increased significantly by the doses of 1.0-20.0 mumol V/100 g, while bone acid phosphatase activity was not altered significantly. Bone DNA content was increased significantly by the dose of 1.0-10.0 mumol V/100 g. Bone calcium content was not altered significantly by administration of vanadium. The increase in serum calcium concentration caused by administration of vanadium (20.0 mumol/100 g) was prevented completely by simultaneous injection of zinc sulfate (15.3 mumol Zn/100 g) for 3 days, although zinc alone did not have any effect. Administration of zinc (15.3 mumol/100 g) produced an appreciable increase in bone alkaline phosphatase activity, DNA content, and calcium content. These increases were not enhanced significantly by simultaneous injection of vanadium (2.0 and 20.0 mumol V/100 g). The present study indicates that a comparatively low dose of vanadium may play a nutritional role in bone formation of weanling rats, and that zinc can prevent the relevation of the toxic effect of vanadium with higher doses.

Acid Phosphatase↗
PubMed1989

Alteration in bone metabolism with increasing age: effects of zinc and vitamin D3 in aged rats.

The alteration in bone metabolism with increasing age was investigated in the femoral diaphysis of male rats. Calcium content was highest in the bone from 3-week-old rats (491 +/- 13 mg/g bone ash), falling gradually with aged to 357 +/- 7 and 306 +/- 9 mg/g bone ash in 28- and 52-week-old rats, respectively. Bone zinc content increased until rats were 3 weeks of age, and thereafter remained constant. Deoxyribonucleic acid (DNA) content was highest in the bone from 1-week-old rats, and it decreased markedly with increasing age. Alkaline phosphatase and acid phosphatase activities increased up to 3 weeks, then subsequently declined with age. Thus, the retardation of bone metabolism was induced by ageing. When zinc sulfate (5.0, 10.0 and 20.0 mg Zn/kg body weight) was administered orally for 3 d to 28-week-old rats, alkaline phosphatase activity and calcium content in the femoral diaphysis was elevated markedly by all doses. The oral administration of vitamin D3 (2.0 and 20 micrograms/kg) for 3 d in 28-week-old rats did not produce an appreciable increase in bone alkaline phosphatase activity or calcium content, while 1,25-dihydroxyvitamin D3 (1.5 micrograms/kg) caused a significant increase in those biochemical indices. These results indicate that zinc and 1,25-dihydroxyvitamin D3 play a role as activators in bone metabolism of ageing rats.

Acid Phosphatase↗
PubMed1989

Effects of Ca2+ and V5+ on glucose-6-phosphatase activity in rat liver microsomes: the Ca2+ effect is reversed by regucalcin.

The effect of regucalcin, a calcium-binding protein isolated from rat liver cytosol, on glucose-6-phosphatase in the microsomes of rat liver was investigated. Addition of Ca2+ up to 2.5 microM to the enzyme reaction mixture caused a significant increase of glucose-6-phosphatase activity in hepatic microsomes, while Ni2+, Zn2+, Cd2+, Cu2+, Mn2+ and Co2+ (20 microM) did not have an appreciable effect. Vanadate (V5+) markedly inhibited the enzyme activity; a significant inhibitory effect was seen at 10 microM V5+. The Ca2+-induced increase of glucose-6-phosphatase activity was reversed by the presence of regucalcin; the effect was complete at 1.0 microM of the protein. Regucalcium had no effect on the basal activity of the enzyme. Meanwhile, the inhibitory effect of V5+ (10-100 microM) on glucose-6-phosphatase was not appreciably blocked by the presence of regucalcin (up to 2.0 microM). The present data suggest that hepatic microsomal glucose-6-phosphatase is uniquely regulated by Ca2+ and V5+, of various metals, and that the Ca2+ effect is reversed by regucalcin. The present study supports the view that regucalcin plays an important role as a regulatory protein in liver cell function related to Ca2+.

Animals↗
PubMed1988

Zinc stimulation of bone protein synthesis in tissue culture. Activation of aminoacyl-tRNA synthetase.

The present investigation was undertaken to clarify the effect of zinc on bone protein synthesis in tissue culture. Calvaria were removed from 3-week-old male rats and cultured for periods up to 96 hr in Dulbecco's Modified Eagle Medium (high glucose, 4500 mg/dl) supplemented with antibiotics and bovine serum albumin. The calvaria were incubated at 37 degrees in 5% CO2/95% air in the medium containing 10(-6)-10(-4) M zinc. Zinc content in bone cells was increased when the culture was treated with 10(-5) and 10(-4) M zinc for 48 hr. When calvaria cultured in the presence of 10(-4) M zinc were pulsed with [14C]uridine, the incorporation of [14C]uridine into the bone RNA was not increased significantly. In the pulse with [3H]leucine, the presence of 10(-5) to 10(-4) M zinc in the medium caused a significant increase in the incorporation of [3H]leucine into the acid-insoluble residues of bone tissue. This increase was blocked completely by treatment with 10(-7) M cycloheximide, an inhibitor of protein synthesis. When [3H]leucine was added into the reaction mixture containing the 5500 g supernatant fraction of the homogenate prepared from calvaria cultured in the presence of 10(-4) M zinc, the in vitro protein synthesis was increased about 2-fold. The activity of [3H]leucyl-tRNA synthetase in the 105,000 g supernatant fraction (cytosol) of the bone homogenate was increased about 2-fold by the culture with 10(-4) M zinc. The presence of 10(-4) M dipicolinate, a specific chelator of zinc, in the culture medium negated the effect of zinc on [3H]leucyl-tRNA synthetase activity. The addition of 10(-7) to 10(-6) M zinc into the reaction mixture containing enzyme extracts obtained from uncultured rat calvaria caused a 2-fold increase of [3H]leucyl-tRNA synthetase activity. These results clearly indicate that zinc induces the stimulation of protein synthesis at the translational level in bone cells. The present study further supports the view that zinc increases protein synthesis in bone cells and that the metal induces bone formation.

Amino Acyl-tRNA Synthetases↗
PubMed1987

Stimulatory effect of zinc on bone formation in tissue culture.

The present investigation was undertaken to clarify the in vitro effect of zinc on bone metabolism in tissue culture. Calvaria were removed from weanling rats (3-week-old males) and cultured for periods up to 96 hr in Dulbecco's Modified Eagle Medium (high glucose, 4500 mg/dl) supplemented with antibiotics and bovine serum albumin. The experimental cultures contained 10(-7) to 10(-3) M zinc sulfate. All cultures were incubated at 37 degrees in 5% CO2/95% air. Zinc uptake by bone was increased significantly in cultures with concentrations of zinc greater than 10(-6) M. Bone calcium content was increased significantly by the presence of 10(-4) M zinc. This increase was blocked by the presence of 10(-6) M cycloheximide. Bone alkaline phosphatase activity was elevated in the presence of zinc (10(-6) to 10(-3) M), but the effect was inhibited by 10(-7) M cycloheximide or 10(-8) M actinomycin D. Zinc (10(-4) M) also significantly increased ATPase activity in the bone, whereas it did not alter significantly by pyrophosphatase, acid phosphatase and beta-N-acetylglucosaminidase activities. Furthermore, bone collagen content was raised by 10(-6) to 10(-4) M zinc. This elevation was prevented by 10(-7) cycloheximide or 10(-8) M actinomycin D. Bone DNA content and [3H]thymidine incorporation by the bone were not altered significantly by 10(-4) M zinc. These findings indicate that the zinc had a direct stimulatory effect on bone mineralization in vitro, and that bone protein synthesis was a necessary component of this response. Zinc may stimulate bone formation in tissue culture.

Alkaline Phosphatase↗
PubMed1987

Changes of phospholipase A2 inhibitory activity in the K+-sensitive actin gelation factor during the differentiation of myeloid leukemia cells.

The phospholipase A2 inhibitory activity of a 38 kDa K+-sensitive actin gelation factor in a murine leukemia cell line (M1) was examined. A specific antibody against 38 kDa protein was found to cross-react with 37 kDa protein (lipocortin) in rat peritoneal exudates. Although the native 38 kDa protein from M1 cells did not block phospholipase A2 activity, pretreatment with alkaline phosphatase produced a form that did inhibit this enzyme. However, a purified 38 kDa protein from differentiated M1 cells blocked phospholipase A2 activity without pretreatment with alkaline phosphatase. Phospholipase A2 inhibitory activity of the 38 kDa protein was not altered by addition of actin. These findings suggest that the phospholipase A2 inhibitory of our 38 kDa protein was induced during differentiation. We also proposed that our 38 kDa protein has the same epitope as lipocortin.

Actins↗
PubMed1986

Effect of essential trace metals on bone metabolism in weanling rats: comparison with zinc and other metals' actions.

The effect of essential trace metals on bone metabolism was investigated in the femoral diaphysis of weanling rats. Oral administration of zinc (1.53-306 mumol/100 g body weight) for 3 days produced significant increases in alkaline phosphatase activity and DNA content. These biochemical indices were also increased by oral administration of chromium (III), cobalt, copper, manganese, and nickel with the dose of 1.53 mumol/100 g. With the dose of 15.3 mumol/100 g of above all metals, except zinc, the enzyme activity was significantly decreased in comparison with control, while DNA content was not decreased significantly. Moreover, the effect of zinc on alkaline phosphatase activity and DNA content was not enhanced by simultaneous administration of other metals (1.53 mumol/100 g). The present study indicates that, of the essential trace metals, zinc can effectively stimulate the bone growth and calcification with comparatively higher dose levels. This suggests a nutritional significance of zinc on bone growth.

Alkaline Phosphatase↗
PubMed1986

Enhancement of in vitro ribonucleic acid synthesis on chromium(III)-bound chromatin.

Z chromatin-chromium (Cr) complex, prepared from mouse liver chromatin and CrCl3, showed a significantly enhanced template activity for in vitro RNA synthesis. Digestion experiments with this complex using micrococcal nuclease and DNase I suggested that Cr(III) preferentially binds to linker regions rather than core regions of chromatin. Further, it was found that Cr(III) binds to DNA and nonhistone proteins (NHP), but hardly to histones. Moreover, the template activity of an NHP-Cr complex, when added to a DNA-histones complex, was inhibited remarkably. The template activity of the chromatin-Cr complex was not significantly altered by proteinase K digestion. Furthermore, experiments using rifampicin and [gamma-32P]guanosine 5'-triphosphate (GTP) demonstrated an increase in the number of initiation sites in the chromatin-Cr complex. These results suggest that, in this in vitro system, Cr(III) preferentially binds to DNA in chromatin and causes an increase in the number of initiation sites, thus enhancing RNA synthesis.

Animals↗
PubMed1986

Increment of prostaglandin E2 in association with elevation of urinary sodium excretion following lead administration.

Lead administered to semi-fasted rats caused an elevation of urinary sodium excretion but no increase of urinary potassium excretion as previously observed in fasted rats. Moreover, in this experiment it was found that urinary and serum prostaglandin E2 (PG E2) contents were increased in association with the elevation of urinary sodium excretion by lead and that natriuresis was suppressed by indomethacine treatment. These findings suggest a stimulation of prostaglandin synthetase rather than to a suppression of the renin-angiotensin-aldosterone system as a primary reaction caused by the lead administration.

Administration, Oral↗
PubMed1985

Changes in adrenal function as a possible mechanism for elevation of serum glucose by a single large dose of fluoride.

Serum glucose was elevated immediately after ip administration of a single large dose of fluoride (NaF 35 mg/kg) to rats. Moreover, elevation of serum glucose following ip administration of 35 mg/kg of fluoride to rats was suppressed by adrenalectomy, dibenamine, or propranolol, but not by thyroid-parathyroidectomy. The elevation of serum glucose was associated with enhancement of glucose-6-phosphatase activities in liver and kidney in fluoride-treated rats.

17-Hydroxycorticosteroids↗