Biomedical subjects

B Enkvetchakul

Publications and source records attributed to B Enkvetchakul.

9 recordsLinked to original sources

PubMed1998

Inhibition of skin carcinomas but not papillomas by sphingosine, N-methylsphingosine, and N-acetylsphingosine.

The sphingoid base backbones of sphingolipids are highly bioactive compounds that affect cell growth, differentiation, diverse cell behaviors, and programmed cell death. Therefore, the efficacy of sphingosine (SPH) and the analogs N-acetylsphingosine (NAS), N-methylsphingosine (NMS), octylamine (OCT), and sterylamine (STR) in the prevention of skin cancer was assessed in female Sencar mice by measuring effects on the induction of epidermal ornithine decarboxylase (ODC) activity and hyperplasia by 12-O-tetradecanoylphorbol-13-acetate (TPA) and effects on the induction of skin tumors by 7, 12-dimethylbenz[a]anthracene (DMBA) and TPA. ODC was measured in the shaved dorsal skin of mice treated topically with 0.05-20 mumol of these compounds 30 minutes before application of 8.5 nmol of TPA in 0.2 ml of acetone. ODC activity was inhibited by > or = 5 mumol of SPH and STR, > or = 10 mumol of NAS and NMS, and 20 mumol of OCT. In contrast, the induction of hyperplasia was not inhibited by application of these compounds 30 minutes before TPA. Two carcinogenesis studies were conducted with 10 nmol of DMBA as the initiator and 3.2 nmol of TPA (2x/wk for 15 wk) as the promoter. In the first study, NAS, NMS, OCT, and STR (0.05 and 0.5 mumol) were applied before each TPA application. Papilloma incidence and multiplicity were not inhibited, but NAS (0.05 mumol) and NMS (0.05 and 0.50 mumol) increased cancer-free survival. In the second experiment, SPH, NAS, and NMS (0.05 and 0.5 mumol) were applied 30 minutes before each TPA treatment and twice weekly for 10 weeks after the final TPA treatment. Papilloma incidence and multiplicity were not inhibited; however, the proportion of mice without carcinoma was increased by both doses of SPH and by 0.5 mumol of NAS. Thus low doses of sphingolipids that were not effective in inhibiting ODC activity, reducing hyperplasia, or preventing epidermal papilloma development were, nonetheless, effective in inhibiting carcinoma development.

Amines↗

PubMed1995

Influence of diethyl maleate and cysteine on tissue glutathione and growth in broiler chickens.

The objectives of this study were to determine the effects of diethyl maleate (DEM) and l-cysteine (L-Cys) on tissue glutathione (GSH) and growth in male broiler chickens. In Experiment 1, broilers were treated with DEM (0, 1.5, 3, 6, or 12.0 mmol/kg BW, i.p.). After 1 h, maximum GSH depletions were to 9, 24, 20, 19, and 35% of control (0 mmol DEM/kg) for liver, lung, kidney, heart, and brain, respectively. In Experiment 2, time-course changes following 1.5 mmol DEM/kg (i.p.) were determined; time-controls received an equal amount of corn oil (CO, .25 mL/kg BW). Levels of GSH in all tissues were low at 1 and 2 h after DEM in comparison to time-control values. Tissue GSH concentrations returned to values that were not different from controls by 5 h in liver and kidney, by 12 h in heart, and by 24 h in brain and lung. In Experiment 3, the effects of feeding a control diet (0% L-Cys) or one supplemented with 1% L-Cys from 3 to 7 wk of age with weekly i.p. injections (at 3,4,5, and 6 wk of age) of DEM (1.5 mmol/kg BW) or CO (.25 mL/kg BW) on growth rate and tissue GSH were determined. There were no differences in BW among treatment groups between 3 and 6 wk of age. Although there were no differences in 7-wk BW between controls (0% L-Cys/CO) and birds treated with DEM fed either diet, the 1% L-Cys/CO group was heavier (P < .05) than either the 0% or 1% L-Cys/DEM groups, and heavier (P = .066) than controls at 7 wk of age. At 5 wk of age, 1% L-Cys raised GSH concentrations in liver, kidney, lung, and duodenum, but had no effect on heart GSH in birds treated with either CO or DEM. Control hepatic GSH concentrations were higher at 7 than at 5 wk of age. With the exception of duodenal GSH in CO birds, 1% L-Cys had no effect on tissue GSH concentrations in 7-wk-old birds. The results of this study provide an initial characterization of GSH metabolism in commercial male broilers and indicate that DEM produced dose- and time-dependent changes in GSH similar to reported changes in mammals. Results of this study also indicate that increased tissue GSH may be beneficial for growth.

Analysis of Variance↗

PubMed1995

Liver and blood glutathione in male broiler chickens, turkeys, and quail.

The objective of the present study was to establish age relationships for hepatic and whole blood glutathione (GSH) in male broiler chickens, quail, and turkeys utilizing lines within each poultry species with different rates of growth. Liver and blood samples were obtained from three quail lines (light, medium, and heavy) at 3 and 6 wk of age, from two turkey lines (light and heavy) at 10 and 20 wk of age, and two broiler lines (medium and heavy) at 3, 5, and 7 wk of age. With the exception of the heavy turkey line, older birds generally exhibited higher hepatic GSH concentrations than younger birds. There was no apparent age-related difference in whole blood GSH, nor was whole blood GSH correlated with hepatic GSH in any poultry species.

Age Factors↗

PubMed1995

Effect of alpha-tocopherol on antioxidants, lipid peroxidation, and the incidence of pulmonary hypertension syndrome (ascites) in broilers.

Research has demonstrated a compromised antioxidant capacity in broilers with pulmonary hypertension syndrome (PHS). Thus, the objective of the present study was to assess the effects of vitamin E on PHS-induced mortality, tissue antioxidants, and plasma lipid peroxides in male broilers. Control broilers were provided normal ventilation but others, maintained under low ventilation conditions to induce PHS, were randomly assigned to nonimplanted (NI), placebo (PL), or vitamin E (VE) implanted groups. The VE implant released a total of 15 mg of alpha-tocopherol from 0 to 3 wk of age. Tissues and blood samples were obtained at 3 and 5 wk of age from birds with (PHS+) and without (PHS-) PHS. Five-week PHS cumulative mortality was lowered by alpha-tocopherol with mortality rates of 3.6, 4.2, 11.9, and 11.8%, for Controls, VE, NI, and PL groups, respectively. The PHS+ birds exhibited lower body weights, higher hematocrit, right ventricular hypertrophy, lower alpha-tocopherol and glutathione (GSH) concentrations in liver and lung, as well as indicators of oxidative stress, including elevated plasma lipid peroxides and lower oxidized GSH in liver and erythrocytes, at 5 wk of age. All birds exhibited lower erythrocyte catalase activity at 5 than at 3 wk of age. An improved antioxidant capacity was observed in VE birds, including higher liver and lung alpha-tocopherol at 3 and 5 wk, higher liver GSH at 3 wk, and lower plasma lipid peroxide values at 5 wk of age. Direct correlations observed between body weight and plasma lipid peroxides at 3 wk (r = .45) and between right ventricular hypertrophy and plasma lipid peroxides at 5 wk (r = .48), suggests that lipid peroxidation plays a role in the etiology of PHS. The results indicate that the VE implant was effective in lowering PHS-induced mortality in broilers apparently by attenuating processes leading to lipid peroxidation.

Analysis of Variance↗

PubMed1995

Pulmonary arteriole hypertrophy in broilers with pulmonary hypertension syndrome (ascites).

Two experiments were conducted to determine the effect of low ventilation or cool temperature environments on pulmonary arteriole hypertrophy. Male broilers were maintained under control or low ventilation conditions in Experiment 1, whereas male broiler breeder by-product chicks were exposed to cool temperature conditions in Experiment 2. Birds were randomly selected for histological evaluation of lung tissue in both experiments. In Experiment 1, birds that had pulmonary hypertension syndrome (PHS+) exhibited a greater degree of inflammation of lung tissue at 5 and 7 wk of age than controls or birds that did not have PHS (PHS-). These PHS+ birds also had higher numbers of cartilaginous osseous nodules at 3 and 7 wk of age than controls. Morphometric analyses revealed that PHS+ birds in Experiment 1 had a thicker medial layer associated with 100 to 200 microns diameter pulmonary arterioles at 7 wk of age, and 50 to 100 microns arterioles at 3 and 7 wk of age than PHS- or control birds. In Experiment 2, PHS+ birds exhibited a thicker medial layer in pulmonary arterioles at 7 wk of age than did PHS- birds, but there were no differences in medial layer thickness at 5 wk of age nor were there differences in the degree of inflammation or amount of osseous nodule formation between PHS+ and PHS- birds at 5 and 7 wk of age. Thus, pulmonary arteriole hypertrophy was observed in birds having PHS in response to both low ventilation and cool temperature environments and this hypertrophy occurred with or without a coincident inflammatory response in lung tissue.

Animals↗

PubMed1993

Prostacyclin elevation following glutathione depletion in vivo. Possible threshold dependency in liver and lung.

The major objective of this study was to determine if a threshold level of glutathione (GSH) depletion is required to elevate plasma prostacyclin (6-ketoPGF1 alpha) in male Sprague-Dawley rats. Rats were treated i.p. with various doses of phorone, diethyl maleate (DEM), or GSH with and without DEM. Similar maximal depletions of hepatic GSH (to 10% of control) and renal GSH (to 50% of control) were observed with DEM and phorone, but lung GSH was depleted maximally by only 30% with phorone compared with a 70% depletion by DEM. Changes in lung GSH, but not kidney GSH, were closely correlated with changes in hepatic GSH 6-KetoPGF1 alpha levels in the lung were 10- to 30-fold higher than in kidney or liver, and there was a stronger correlation between lung and plasma 6-ketoPGF1 alpha than with the other two tissues. The increase in lung 6-ketoPGF1 alpha following GSH depletion did not appear to be due to a shift in prostaglandin metabolite synthesis since reciprocal changes in PGE2 were not observed; lung PGE2 levels were largely unaffected by DEM or phorone. Both DEM and phorone elevated plasma 6-ketoPGF1 alpha but the magnitude of increase for DEM (5- to 6-fold) was much greater than the 2-fold increase for phorone. The increase in plasma 6-ketoPGF1 alpha by 1.0 mL DEM/kg was attenuated by simultaneous administration of 2 mmol GSH/kg. The results indicate that the lung may be responsible for increases in plasma 6-ketoPGF1 alpha following GSH depletion and that a critical level of GSH depletion in the liver and/or lung may be necessary to elevate plasma 6-ketoPGF1 alpha levels.

6-Ketoprostaglandin F1 alpha↗

PubMed1993

Compromised antioxidant status associated with ascites in broilers.

Tissue infiltration by white blood cells in poultry with ascites has been reported, which could alter endogenous antioxidant status from oxidant stress. Therefore, the objective of this study was to determine the effect of ascites on ascorbic acid, tocopherol, and glutathione (GSH), which are major intracellular antioxidants. Broiler chicks (1 day) were placed in environmental chambers maintained with normal ventilation (Control) or under low ventilation, which produced a cumulative mortality of 31.3% due to ascites. At 3, 5, and 7 wk, lung and liver tissues were obtained from control birds (n = 5) and from birds in the low ventilation chamber with (ASC, n = 5) or without (NASC, n = 5) overt symptoms of ascites. There were no differences in tissue ascorbate, tocopherol, and GSH between the control and NASC groups with the exception of hepatic tocopherol at 7 wk, which was higher (P < .05) in NASC birds than in ASC and control birds. In general, lung and liver concentrations of all three antioxidants were lower (P < .05) in ASC birds than in NASC and control groups. Uric acid, a product of purine metabolism, was lower (P < .05) in liver and lung in ASC birds at 3 wk compared with control birds. However, uric acid concentrations in ASC birds were higher (P < .05) in the lung and serum at 5 wk, and in the liver at 7 wk compared with NASC and control birds.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Influences of sphingosine on two-stage skin tumorigenesis in Sencar mice.

Sphingosine (SPH) was studied as an inhibitor of skin tumor promotion in skin cancer initiated by 7,12-dimethylbenz[a]-anthracene (DMBA) and promoted by 12-O-tetradecanoylphorbol-13-acetate (TPA). Two tumorigenesis studies were conducted using female Sencar mice treated with 10 nmol DMBA in 0.2 ml acetone at 8 weeks of age and promoted beginning 1 week later with 3.2 nmol TPA applied twice per week. In the high-dose study, 10 mumol SPH was applied 30 min before each TPA treatment. The low-dose study used 0.5, 0.05, or 0.01 mumol treatments with SPH 30 min before TPA. In the high-dose study SPH treatment alone following initiation by DMBA, and SPH treatment preceding TPA in DMBA-initiated mice accelerated the development of papillomas in comparison with the DMBA/TPA-treated group. The low-dose experiment showed no consistent alteration of tumorigenesis by SPH in the DMBA/TPA-treated groups, and low doses of SPH following DMBA did not promote skin tumorigenesis. SPH treatment did not alter body weight in either experiment.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1989

Inhibition of the induction of ornithine decarboxylase activity by 12-O-tetradecanoylphorbol-13-acetate in mouse skin by sphingosine sulfate.

We investigated the effect of sphingosine sulfate on the induction of ODC (ornithine decarboxylase) activity by TPA (12-O-tetradecanoylphorbol-13-acetate) in mouse skin. When applied topically to the shaved skin of SENCAR mice at dosages of 10-40 mumol per animal, 30 min before the superficial application of 8.5 nmol of TPA, sphingosine sulfate dramatically inhibited the induction of ODC activity by the tumor promoter. Significant inhibition of TPA-induced ODC activity was observed at 4, 6 and 8 h after TPA treatment in separate studies. The results indicate that sphingosine sulfate is an effective inhibitor of ODC induction by TPA in mouse skin.

Animals↗