• KSBB Journal
• /
• v.11 no.3
• /
• pp.276-287
• /
• 1996

Batch suspension cultures of hybridoma cell were performed with various initial glutamine concentrations to investigate the effects of glutamine on cell growth and death, monoclonal antibody production, glucose and glutamine consumption, and the production of lactate and ammonium ion. An mathematical kinetic model was formulated to describe the kinetics of cell growth, the consumption of nutrients (glucose and glutamine), and the production of monoclonal antibody and waste metabolites (lactate and ammonium ion) based on experimental data. An equation for the specific growth rate was developed such that superimposed Monod equation in glucose and glutamine, with non-competitive type inhibition relations in ammonium ion and lactate. The inhibition constant for lactate was inversely proportional to the lactate concentration. The specific death rate was considered to be a function of glucose, glutamine, ammonium ion and lactate concentration.

• Journal of Life Science
• /
• v.23 no.6
• /
• pp.832-837
• /
• 2013

In this study, it was investigated the possible mechanisms by which glutamine deprivation exerts its anti-proliferative action in cultured human prostate carcinoma PC3 cells. Glutamine deprivation resulted in inhibition of growth and G2/M arrest of the cell cycle in a time-dependent manner without apoptosis induction, as determined by MTT assay, DAPI staining and flow cytometry analyses. The induction of G2/M arrest by glutamine deprivation was associated with the inhibition of expression of Cdc2, cyclin A and cyclin B1, and up-regulation of the expression of cyclin-dependent kinase (Cdk) inhibitor p21(WAF1/CIP1) in both transcriptional and translational levels. Moreover, glutamine deprivation increased the phosphorylation of checkpoint kinase (Chk)1 and Chk2; however, the levels of Cdc25C phosphorylation were decreased in response to glutamine deprivation in a time-dependent manner. Our data provide a first biochemical evidence that glutamine deprivation suppresses cell viability through G2/M phase arrest without induction of apoptosis in PC3 cells.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.42 no.8
• /
• pp.1167-1174
• /
• 2013

Cancer cells exhibit increased demand for glutamine-derived carbons to support anabolic processes. Indeed, the spectrum of glutamine-dependent tumors and the mechanisms through which glutamine supports cancer metabolism remain areas of active investigation. In the present study, we investigated the effects of glutamine deprivation on the correlation between tightening of tight junctions (TJs) and anti-invasive activity in human prostate carcinoma LnCap cells. Glutamine deprivation markedly inhibited cell motility and invasiveness in a time-dependent manner. The anti-invasive activity of glutamine deprivation was associated with an increased tightness of the TJ, which was demonstrated by an increase in transepithelial electrical resistance (TER). The activities of matrix metalloproteinase (MMP)-2 and MMP-9 were inhibited in a time-dependent fashion by glutamine deprivation, which was correlated with a decrease in expression of their mRNA and proteins and up-regulation of tissue inhibitors of metalloproteinases (TIMPs) expression. Furthermore, glutamine deprivation repressed the levels of the claudin family members, which are major components of TJs that play a key role in the control and selectivity of paracellular transport. Moreover, the levels of E-cadherin, a type I transmembrane glycoprotein, and snail, an epithelial to mesenchymal transition regulator and zinc finger transcription factor, were markedly modulated by glutamine deprivation. Taken together, these findings suggest that TJs and MMPs are critical targets of glutamine deprivation-induced anti-invasion in human prostate carcinoma LnCap cells.

• Journal of Life Science
• /
• v.23 no.7
• /
• pp.926-932
• /
• 2013

Glutamine and serum are essential for cell survival and proliferation in vitro, yet the signaling pathways that sense glutamine and serum levels in endothelial cells remain uninvestigated. In this study, we examined the effects of glutamine deprivation and serum starvation on the fate of endothelial cells using a human umbilical vein endothelial cell (HUVEC) model. Our data indicated that glutamine deprivation and serum starvation trigger a progressive reduction in cell viability through apoptosis induction in HUVECs as determined by DAPI staining and flow cytometry analysis. Although the apoptotic effects were more predominant in the glutamine deprivation condition, both apoptotic actions were associated with an increase in the Bax/Bcl-2 (or Bcl-xL) ratio, down-regulation of the inhibitor of apoptosis protein (IAP) family proteins, activation of caspase activities, and concomitant degradation of poly (ADP-ribose) polymerases. Moreover, down-regulation of the expression of Bid or up-regulation of truncated Bid (tBid) were observed in cells grown under the same conditions, indicating that glutamine deprivation and serum starvation induce the apoptosis of HUVECs through a signaling cascade involving death-receptor-mediated extrinsic pathways, as well as mitochondria-mediated intrinsic caspase pathways. However, apoptosis was not induced in cells grown in glutamine- and serum-free media when compared with cells exposed to glutamine deprivation or serum starvation alone. Taken together, our data indicate that glutamine deprivation and serum starvation suppress cell viability without apoptosis induction in HUVECs.

• Journal of the Korean Chemical Society
• /
• v.34 no.6
• /
• pp.622-628
• /
• 1990

The bio-sensor for glutamine has been constructed by immobilizing petal of the rose structural elements on an ammonia gas sensor. This sensor was investigated for the effects of pH, temperature, buffer solution, tissular amounts, interferences and lifetime. As a result, the tissue sensor showed linear range of $8.0 {\times} 10^{-4}$ ∼$5.0 {\times} 10^{-2}$ M glutamine with a slope of 52 mV/decade in pH 7.8, 0.2M phosphate beffer solution at 37$^{\circ}C$. The tissular amounts used for this sensor was 50 mg. This sensorr showed excellent selectivity. This sensor was compared with other structural elements of rose. Actually, this tissue sensor appeared to be very useful for the determination of glutamine.

• Clinical and Experimental Pediatrics
• /
• v.48 no.4
• /
• pp.425-432
• /
• 2005

Purpose : Polyglutamine diseases are a group of diseases caused by the expansion of a polyglutamine tract in the protein. The present study was performed to verify if polyglutamine disease transgenic Drosophila models show similar dysfunctions as are seen in human patients. Methods : Polyglutamine disease transgenic Drosophila were tested for their climbing ability. And using genetic methods, the effects of anti-apoptotic gene bcl-2 and chemical chaperones on neurodegeneration were observed. Also, spinocerebellar ataxia 2 (SCA2) transgenic Drosophila lines were generated for future studies. Results : Expanded forms of spinocerebellar ataxia 3 (SCA3) transgenic protein causes characteristic locomotor dysfunction when expressed in the nervous system of Drosophila but the anti-apoptotic gene bcl-2 shows no evidence of ameliorating the deleterious effect of the expanded protein. However, Glycerol, a chemical chaperone, seemed to reduce the toxicity, at least in the eyes of the transgenic flies. The level SCA2 expression is too weak in the transgenic SCA2 Drosophila for evaluation. Conclusion : SCA3 transgenic Drosophila show ataxic behavior as observed in human patients. Chemical chaperones such as glycerol may prove beneficial in this class of genetic disease, which has no current method of cure.

• Journal of Nutrition and Health
• /
• v.36 no.7
• /
• pp.711-719
• /
• 2003

The effects of taurine, carnitine or glutamine supplementation on endurance exercise performance along with related fatigue factors were evaluated in male college students in the Department of Physical Education, who's maximal oxygen consumption rates (VO$_2$max) were equivalent to those of endurance athletes. Twenty four subjects were randomly divided into 4 groups (n=6), and given placebo, taurine (4 g/day), carnitine (4 g/day), or glutamine (4 g/day) tablets for 2 weeks. Subjects could run 6.9 min or 9.0 min longer until exhausted on a treadmill at the intensity of 75% VO$_2$max following taurine or camitine supplementation for 2 weeks, respectively, compared to the value measured prior to each supplementation. Glutamine or placebo supplementation did not improve the endurance exercise performance based on the running time until exhausted on a treadmill. Serum lactate concentrations measured 1 hr after the initiation of the endurance exercise, as well as at all-out state tended to be decreased by taurine, carnitine, or glutamine supplementation, and were significantly lowered (43% decrease) by carnitine supplementation (p < 0.05). Taurine supplementation significantly reduced the serum inorganic phosphorus concentration measured at all-out state (14% decrease, p < 0.05), while carnitine supplementation significantly lowered the resting state serum inorganic phosphorus level (20% decrease, p < 0.05). Taurine (32% reduction) or carnitine (23% reduction) supplementation significantly decreased serum ammonia concentration measured at all-out state (p < 0.05). From these results, 4 g/day of taurine or carnitine supplementation appears to improve the endurance exercise performance and related human fatigue factors.

• Microbiology and Biotechnology Letters
• /
• v.2 no.1
• /
• pp.51-55
• /
• 1974

• Proceedings of the Korean Nutrition Society Conference
• /
• 2000.06a
• /
• pp.133-133
• /
• 2000

• Proceedings of the Korean Nutrition Society Conference
• /
• 2002.11a
• /
• pp.110-110
• /
• 2002