• Korean Journal of Veterinary Research
• /
• v.41 no.3
• /
• pp.319-325
• /
• 2001

Several recent studies demonstrate that cAMP accumulation evokes marked changes in magnesium ($Mg^{2+}$) homeostasis. The goal of this study was to investigate the effect of melatonin, the principal hormone of the vertebral pineal gland, on $Mg^{2+}$ regulation in perfused guinea pig hearts. We hypothesized that melationin would regulate $Mg^{2+}$ efflux induced by adrenergic drugs and cAMP analogues because melatonin inhibites adneylate cyclase (AC) and phospholipase C(PLC) in the hearts. The $Mg^{2+}$ content in the perfusate was significantly higher in the presence than in the absence of melatonin. The addition of forskolin, isoproterenol or dimaprit to perfused hearts induced a marked $Mg^{2+}$ efflux. These effluxes were not inhibited by melatonin. The $Mg^{2+}$ efflux could also be induced by phenylephrine, a ${\alpha}_1$-adrenoceptor agonist. This phenylephrine-induced $Mg^{2+}$ efflux was inhibited by melatonin. In addition, the phenylephrine-induced $Mg^{2+}$ efflux was potentiated by PMA, a protein kinase C(PKC) activator. This $Mg^{2+}$ efflux was inhibited by melatonin. In conclusion, these data suggest that melatonin regulates $Mg^{2+}$ homeostasis and the inhibitory effect of melatonin on ${\alpha}_1$-adrenoceptor-stimulated $Mg^{2+}$ efflux may occur through an inhibition of PLC pathway in perfused guinea pig hearts.

• Korean Journal of Veterinary Research
• /
• v.39 no.3
• /
• pp.463-471
• /
• 1999

Magnesium($Mg^{2+}$) is one of the most abundant intracellular divalent cation. Although recent studies demonstrate that adrenergic receptor stimulation evokes marked changes in $Mg^{2+}$ homeostasis, the regulation of $Mg^{2+}$ by dopaminergic receptor stimulation is not yet known. In this work, we used dopaminergic agents to identify which type(s) of receptors were involved in the mobilization of $Mg^{2+}$ by dopaminergic receptor stimulation in the perfused rat hearts, isolated myocytes and circulating blood. The $Mg^{2+}$ content was measured by atomic absorbance spectrophotometry. Dopamine(DA), apomorphine(APO) and pergolide stimulated $Mg^{2+}$ efflux in the perfused rat hearts and these effects were inhibited by haloperidol or fluphenazine, nonselective dopaminergic antagonists. SKF38393, a selective doparminergic agonist, increased $Mg^{2+}$ efflux from the perfused hearts in dose dependant manners and SKF38393-induced $Mg^{2+}$ efflux was blocked by haloperidol. However, dopaminergic agonists-induced $Mg^{2+}$ efflux was potentiated in the presence of sulpiride or eticlopride, $D_2$-selective antagonist, from the perfused hearts. This increase of $Mg^{2+}$ efflux was blocked by haloperidol or imipramine. DA or pergolide increased in circulating $Mg^{2+}$ from blood. By contrast, PPHT stimulated $Mg^{2+}$ influx(a decrease in efflux) from the perfused hearts and circulating blood. PPHT-induced $Mg^{2+}$ influx was blocked by fluphenazine in the perfused hearts. DA-stimulated $Mg^{2+}$ efflux was inhibited by dopaminergic antagoinst in the isolated myocytes. In conclusion, the flux of $Mg^{2+}$ is modulated by DA receptor activation in the rat hearts. The efflux of $Mg^{2+}$ can be increased by $D_1$-receptor stimulation and decreased by $D_2$-receptor stimulation, respectively.

• Journal of Korean Society of Forest Science
• /
• v.98 no.2
• /
• pp.183-188
• /
• 2009

It is necessary to determine the amount of carbon dioxide ($CO_2$) absorbed by plants and released from forest floor into atmosphere, to gain a better understanding how forests participate in the global carbon cycle. Soil $CO_2$ efflux, litter production, and decomposition were investigated in Q. variabilis and P. densiflora stands in the vicinity of Gwangju, Chonnam province. Soil $CO_2$ efflux was measured using Infrared Gas Analyzer (IRGA) at midday of the 10th day at every month over 12-month period, to quantify seasonal and annual budgets of soil $CO_2$ efflux. Soil temperature and soil moisture were measured at the same time. Seasonal soil $CO_2$ efflux in Q. variabilis and P. densiflora were the highest in summer season. In August, maximum soil $CO_2$ efflux in Q. variabilis and P. densiflora was 7.49, $4.61CO_2{\mu}mol{\cdot}m^{-2}{\cdot}s^{-1}$, respectively. Annual $CO_2$ efflux in each stand was 1.77, $1.67CO_2kg{\cdot}m^{-2}$ respectively. Soil $CO_2$ efflux increased exponentially with soil temperature and related strongly in Q. variabilis ($r^2$=0.96), and in P. densiflora ($r^2$=0.91). Litter production continued throughout the year, but showed a peak on November and December. Annual litter production in the Q. variabilis and P. densiflora stands were $613.7gdw{\cdot}m^{-2}{\cdot}yr^{-1}$ and $550.5gdw{\cdot}m^{-2}{\cdot}yr^{-1}$.$yr^{-1}$, respectively. After 1 year, % remaining mass of Q. variabilis and P. densiflora litter was 48.2, 57.1%, respectively. The soil $CO_2$ efflux rates in this study showed clear seasonal variations. In addition, the temporal variation in the $CO_2$ efflux rates was closely related to the soil temperature fluctuation rather than to variations in the soil moisture content. The range of fluctuation of soil $CO_2$ efflux and litter decomposition rate showed similar seasonal changes. The range of fluctuation of soil $CO_2$ efflux and litter decomposition rate was higher during summer and autumn than spring and winter.

• The Korean Journal of Physiology and Pharmacology
• /
• v.2 no.1
• /
• pp.49-54
• /
• 1998

$Mg^{2+}$ is an important regulator of many cardiac functions. However, regulation of intracellular $Mg^{2+}$ activity in the heart is not well characterized. To assess the effect of histamine $H_2$-receptor stimulation on intracellular $Mg^{2+}$ regulation, changes in extracellular $Mg^{2+}$ concentration were examined under a variety of conditions in perfused guinea pig hearts. $Mg^{2+}$ in the cardiac perfusate was measured by atomic absorbance spectrophotometry. The histamine ($10^{-6}$ M) inuced a marked $Mg^{2+}$ efflux from the heart. The $H_2$-receptor antagonists, cimetidine ($10^{-6}$ M), ranitidined ($10^{-5}$ M), but not a H1-receptor antagonist, diphenhydramine ($3{\times}10^{-6}$ M), completely blocked the histamine-induced $Mg^{2+}$ efflux. The $Mg^{2+}$ efflux could also be induced by forskolin ($3{\times}10^{-6}$ M), 8-Cl-cAMP ($2{\times}10^{-4}$ M), permeable cAMP analogue, or dimaprit, ($10^{-5}$ M). However, the carbachol ($10^{-5}$ M) considerably decreased the efflux of $Mg^{2+}$. In the presence of papaverine ($10^{-5}$ M), a phosphodiesterase inhibitor, dimaprit-induced $Mg^{2+}$ efflux was potentiated. These results suggest that a significant $Mg^{2+}$ efflux from perfused guinea pig heart by histamine can be induced by the histamine $H_2$-receptor stimulation and it is suggested that cytosolic cAMP may be linked.

• Korean Journal of Veterinary Research
• /
• v.39 no.1
• /
• pp.62-69
• /
• 1999

Although it has been reported that hormones or chemicals, which increase in intracellular cAMP, produced $Mg^{2+}$ release from the heart, it is not well characterized whether a specific $Mg^{2+}$ exchanger is involved in cAMP-induced $Mg^{2+}$ efflux in the mammalian hearts. In this work, we studied the relationship between the increase in intracellular cAMP and ion transport system on $Mg^{2+}$ regulation in the perfused rat heart and isolated myocytes. The $Mg^{2+}$ content in the perfusate and supernatant were measured by atomic absorption spectrophotometer. The addition of membrane permeable cAMP analogue to the perfused hearts and myocytes induced a $Mg^{2+}$ efflux in the dose dependent manners. $Mg^{2+}$ efflux was stimulated by cAMP modulators (forskolin, IBMX and Ro20-1724) in the perfused hearts and myocytes. cAMP-induced $Mg^{2+}$ efflux was inhibited by $H_7$, benzamil or imipramine in the perfused hearts and myocytes, but not by EIPA. We confirmed that a significant $Mg^{2+}$ efflux was induced by an increase in intracellular cAMP in the hearts and myocytes. The cAMP-induced increase of $Mg^{2+}$ efflux in the hearts may be involved in ion transport system ($Na^+-Ca^{2+}$ and $Na^+-Mg^{2+}$ exchanger).

• Archives of Pharmacal Research
• /
• v.18 no.3
• /
• pp.173-178
• /
• 1995

Ciprofloxacin resistance mechanisms were studied by investigating the inhibitory effect of ciprofloxacin on the gyrase-mediated DNA supercoiling and the intracellular accumulation of ciprofloxacin in clinical isolates of Pseudomonas aeruginosa. A higher amount of ciprofloxacin was required to inhibit the gyrases purified from the ciprofloxacin-resistant strains than that from the sensitive strain. Reconstitution of heterologous gyrase subunits from different strains revealed alterations in the A and/or the B subunits of gyrase in these strains. In addition, the resistant strains accumulated approximately a half amount of ciprofloxacin inside the cells, compared to the sensitive strain. However, when the active efflux was blocked by carbonyl cyanide m-chlorophenyl hydrazone treatment, intracellular concentration of ciprofloxacin was elevated about 4-7 fold in these strains, while the sensitive strain was not significantly affected by this treatment, indicating that the ciprofloxacin-resistant strains developed a drug efflux system. Interestingly, these resistant strains expressed an envelope protein of approximately 51 kD. These studies suggest that alterations in the gyrase as well as the active drug-efflux system conferred dual ciprofloxacin resistance mechanisms to these clinical isolates of P. aeruginosa.

• BMB Reports
• /
• v.53 no.11
• /
• pp.588-593
• /
• 2020

The accumulation of triglycerides (TGs) in macrophages induces cell death, a risk factor in the pathogenesis of atherosclerosis. We had previously reported that TG-induced macrophage death is triggered by caspase-1 and -2, therefore we investigated the mechanism underlying this phenomenon. We found that potassium efflux is increased in TG-treated THP-1 macrophages and that the inhibition of potassium efflux blocks TG-induced cell death as well as caspase-1 and -2 activation. Furthermore, reducing ATP concentration (known to induce potassium efflux), restored cell viability and caspase-1 and -2 activity. The activation of pannexin-1 (a channel that releases ATP), was increased after TG treatment in THP-1 macrophages. Inhibition of pannexin-1 activity using its inhibitor, probenecid, recovered cell viability and blocked the activation of caspase-1 and -2 in TG-treated macrophages. These results suggest that TG-induced THP-1 macrophage cell death is induced via pannexin-1 activation, which increases extracellular ATP, leading to an increase in potassium efflux.

• BMB Reports
• /
• v.39 no.5
• /
• pp.556-559
• /
• 2006

The Bcl-2 family of proteins regulates mitochondrial functions during cell death by modulating the efflux of death-promoting proteins such as cytochrome c and endonuclease G. Upon the binding of death ligands to their receptors, caspase-8 cleaves Bid, a BH3-only protein, into tBid that causes the mitochondrial damages resulting in the release of cytochrome c and endonuclease G. Also, another BH3-only protein, hNoxa, has been shown to induce the efflux of cytochrome c from the mitochondria. Whether the efflux proteins from the mitochondria in response to tBid or hNoxa are the same or different, however, has not been addressed. We have demonstrated that endonuclease G activities are not detectable among the proteins released from isolated mitochondria by hNoxa but are detectable in that by tBid. These results suggest that the efflux of proteins from the mitochondria are differentially modulated by tBid and hNoxa.

• Journal of Ecology and Environment
• /
• v.37 no.3
• /
• pp.113-122
• /
• 2014

The purpose of this study is to compare soil $CO_2$ efflux between burned and unburned sites dominated by Pinus densiflora forest in the Samcheok area where a big forest fire broke out along the east coast in 2000 and to measure soil $CO_2$ efflux and environmental factors between March 2011 and February 2012. Soil $CO_2$ efflux was measured with LI-6400 once a month; the soil temperature at 10 cm depth, air temperature, and soil moisture contents were measured in continuum. Soil $CO_2$ efflux showed the maximum value in August 2011 as 417.8 mg $CO_2m^{-2}h^{-1}$ (at burned site) and 1175.1 mg $CO_2m^{-2}h^{-1}$ (at unburned site), while it showed the minimum value as 41.4 mg $CO_2m^{-2}h^{-1}$ (at burned site) in December 2011 and 42.7 mg $CO_2m^{-2}h^{-1}$ (at unburned site) in February 2012. The result showed the high correlation between soil $CO_2$ efflux and the seasonal changes in temperature. More specifically, soil temperature showed higher correlation with soil $CO_2$ efflux in the burned site ($R^2$ = 0.932, P < 0.001) and the unburned site ($R^2$ = 0.942, P < 0.001) than the air temperature in the burned site ($R^2$ = 0.668, P < 0.01) and the unburned site ($R^2$ = 0.729, P < 0.001). $Q_{10}$ values showed higher sensitivity in the unburned site (4.572) than in the burned site (2.408). The total soil $CO_2$ efflux was obtained with the exponential function between soil $CO_2$ efflux and soil temperature during the research period, and it showed 2.5 times higher in the unburned site (35.59 t $CO_2ha^{-2}yr^{-1}$, 1 t = $10^3$ kg) than in the burned site (14.69 t $CO_2ha^{-2}yr^{-1}$).

• Nutrition Research and Practice
• /
• v.1 no.3
• /
• pp.200-205
• /
• 2007

The effects of taurine on plasma and liver cholesterol, erythrocyte ouabain sensitive Na efflux and platelet aggregation were examined in Sprague Dawley rats fed control or 0.5% cholesterol with 0.2% cholate diet. Plasma and liver levels of total cholesterol were increased significantly (p<0.05) in rats fed cholesterol diet compared to the control, and taurine significantly decreased the elevated plasma level of cholesterol in rats fed cholesterol diet (p<0.05). HDL-cholesterol was decreased in groups fed the cholesterol diet regardless of taurine supplementation and the difference between groups with and without cholesterol was significant (p<0.01). Plasma triglyceride was decreased and liver triglyceride was increased both significantly (p<0.05) in rats fed cholesterol compared to the control. Plasma and liver triglyceride in rats fed taurine was decreased significantly compared to the control (p<0.05). Intracellular Na tended to be lower in rats fed cholesterol or taurine and higher in rats fed cholesterol plus taurine compared to the control. Na efflux through Na-K ATPase and the passive leak of Na was somewhat reduced in rats fed cholesterol or taurine and was augmented in rats fed cholesterol plus taurine compared to the control, which showed a similar trend to the intracellular Na. Taurine supplementation caused a suppression of Na efflux in groups fed control diet and restored the suppressed Na efflux in groups fed cholesterol. Platelet aggregation was significantly decreased in the group fed taurine compared to the control (p<0.05) and the group fed cholesterol plus taurine was also a little lower in aggregation than the group fed cholesterol. Microscopic examination showed that taurine prevented fatty liver in rats fed cholesterol diet. Taurine known for stimulating Na-K ATPase in some cell types rather decreased erythrocyte ouabain sensitive Na-K ATPase in the present study. Taurine had hypolipidemic and hypocholesterolemic effects and inhibited platelet aggregation which may be favorable for prevention of cardiovascular diseases.