• Asian-Australasian Journal of Animal Sciences
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• v.20 no.5
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• pp.742-747
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• 2007

In order to investigate the mechanism of adaptation to long-term heat stress, six female buffalo calves of about 7 to 8 months age, were exposed to the cool-comfort environment (THI 65) for 21 days to obtain normal values of blood acid-base. An adaptive response of acid-base regulation was determined to long term (21 days) exposure of buffalo calves to hot-dry (THI 80) and hot-humid (THI 84) conditions. Higher rectal temperature and respiratory rate was recorded under hot-humid exposure compared to hot-dry. Significant reduction in the rectal temperature and respiratory rate on day 21 of hot-dry exposure indicated early thermal adaptation compared to hot-humid. Decreasing rectal temperature and respiratory rate from day 1 to 21 was associated with concurrent decrease in blood pH and pCO2. Increased plasma chloride concentration with low base excess in blood and in extracellular fluid suggested compensatory response to respiratory alkalosis. Reduced fractional excretion of sodium with increased fractional excretion of potassium and urine flow rate indicated renal adaptive response to heat stress.

• Journal of Medicine and Life Science
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• v.20 no.3
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• pp.135-138
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• 2023

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.3
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• pp.211-216
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• 2014

Endoplasmic reticulum (ER) stress, unfolded protein response (UPR), and mitochondrial biogenesis were assessed following varying intensities of exercise training. The animals were randomly assigned to receive either low- (LIT, n=7) or high intensity training (HIT, n=7), or were assigned to a control group (n=7). Over 5 weeks, the animals in the LIT were exercised on a treadmill with a $10^{\circ}$ incline for 60 min at a speed of 20 m/min group, and in the HIT group at a speed of 34 m/min for 5 days a week. No statistically significant differences were found in the body weight, plasma triglyceride, and total cholesterol levels across the three groups, but fasting glucose and insulin levels were significantly lower in the exercise-trained groups. Additionally, no statistically significant differences were observed in the levels of PERK phosphorylation in skeletal muscles between the three groups. However, compared to the control and LIT groups, the level of BiP was lower in the HIT group. Compared to the control group, the levels of ATF4 in skeletal muscles and CHOP were significantly lower in the HIT group. The HIT group also showed increased PGC-$1{\alpha}$ mRNA expression in comparison with the control group. Furthermore, both of the trained groups showed higher levels of mitochondrial UCP3 than the control group. In summary, we found that a 5-week high-intensity exercise training routine resulted in increased mitochondrial biogenesis and decreased ER stress and apoptotic signaling in the skeletal muscle tissue of rats.

• Environmental Analysis Health and Toxicology
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• v.21 no.3 s.54
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• pp.275-282
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• 2006

In order to get insight into the mechanism of cadmium (Cd)-induced brain injury, we investigated the effects of Cd on the induction of COX-2 in bEnd.3 mouse brain endothelial cells. Cd induced COX-2 expression and $PGE_2$ release, which were attenuated by thiol-reducing antioxidant N-acetylcysteine (NAC) indicating oxidative components might contribute to these events. Indeed, Cd increased cellular reactive oxygen species (ROS) level and DNA binding activity of nuclear factor-kB (NF-kB), an oxidative stress sensitive transcription factor. Cd-induced $PGE_2$ production and COX-2 expression were significantly attenuated by Bay 11 7082, a specific inhibitor of NF-kB and by SB203580, a specific inhibitor of p38 mitogen activated protein kinase (MAPK). These data suggest that Cd induces COX-2 expression through activation of NF-kB and p38 MAPK, the oxidative stress-sensitive signaling molecules, in brain endothelial cells.

• 한국약용작물학회:학술대회논문집
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• 2007.05a
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• pp.257-258
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• 2007

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.6
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• pp.377-384
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• 2010

The present study examined whether metformin treatment prevents isoporterenol-induced cardiac hypertrophy in mice. Chronic subcutaneous infusion of isoproterenol (15 mg/kg/24 h) for 1 week using an osmotic minipump induced cardiac hypertrophy measured by the heart-to-body weight ratio and left ventricular posterior wall thickness. Cardiac hypertrophy was accompanied with increased interleukin-6 (IL-6), transforming growth factor (TGF)-${\beta}$, atrial natriuretic peptide (ANP), collagen I and III, and matrix metallopeptidase 2 (MMP-2). Coinfusion of metformin (150 mg/kg/24 h) with isoproterenol partially inhibited cardiac hypertrophy that was followed by reduced IL-6, TGF-${\beta}$, ANP, collagen I and III, and MMP-2. Chronic subcutaneous infusion of metformin did not increase AMP-activated protein kinase (AMPK) activity in heart, although acute intraperitoneal injection of metformin (10 mg/kg) increased AMPK activity. Isoproterenol increased nitrotyrosine levels and mRNA expression of antioxidant enzyme glutathione peroxidase and metformin treatment normalized these changes. These results suggest that metformin inhibits cardiac hypertrophy through attenuating oxidative stress.

• Plant Biotechnology Reports
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• v.5 no.1
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• pp.89-103
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• 2011

Two rice varieties, viz. Nonabokra and Pokkali, have been evaluated for their responses to salinity in terms of some physiological and biochemical attributes. During the exposure to salinity (200 mM concentration of sodium chloride for 24, 48, and 72 h), a significant increase in sodium was recorded which was also concomitant with the changes of other metabolic profiles like proline, phenol, polyamine, etc. The protein oxidation was significantly increased and also varied between the two cultivars. The changes in activities of anti-oxidative enzymes under stress were significantly different to the control. The detrimental effects of salinity were also evident in terms of lipid peroxidation, chlorophyll content, protein profiles, and generation of free radicals; and these were more pronounced in Pokkali than in Nonabokra. The assessment and analysis of these physiological characters under salinity could unravel the mechanism of salt responses revealed in this present study and thus might be useful for selection of tolerant plant types under the above conditions of salinity.

• Proceedings of The Korean Society of Agricultural and Forest Meteorology Conference
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• 2019.08a
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• pp.220-220
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• 2019

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.3
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• pp.127-132
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• 2010

Reactive oxygen species (ROS), which include hydrogen peroxide ($H_2O_2$), the superoxide anion (${O_2}^-{\cdot}$), and the hydroxyl radical ($OH{\cdot}$), are generated as by-products of oxidative metabolism in cells. The cerebral cortex has been found to be particularly vulnerable to production of ROS associated with conditions such as ischemia-reperfusion, Parkinson's disease, and aging. To investigate the effect of ROS on inhibitory GABAergic synaptic transmission, we examined the electrophysiological mechanisms of the modulatory effect of $H_2O_2$ on GABAergic miniature inhibitory postsynaptic current (mIPSCs) in mechanically isolated rat cerebral cortical neurons retaining intact synaptic boutons. The membrane potential was voltage-clamped at -60 mV and mIPSCs were recorded and analyzed. Superfusion of 1-mM $H_2O_2$ gradually potentiated mIPSCs. This potentiating effect of $H_2O_2$ was blocked by the pretreatment with either 10,000-unit/mL catalase or $300-{\mu}M$ N-acetyl-cysteine. The potentiating effect of $H_2O_2$ was occluded by an adenylate cyclase activator, forskolin, and was blocked by a protein kinase A inhibitor, N -(2-[p-bromocinnamylamino] ethyl)-5-isoquinolinesulfonamide hydrochloride. This study indicates that oxidative stress may potentiate presynaptic GABA release through the mechanism of cAMP-dependent protein kinase A (PKA)-dependent pathways, which may result in the inhibition of the cerebral cortex neuronal activity.

• International Journal of Industrial Entomology and Biomaterials
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• v.28 no.2
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• pp.85-91
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• 2014

This study was designed to find out the effect of Nosema spore on oxidative damages and antioxidant defence in the midgut of tasar silkworm Antheraea mylitta. Higher level of lipid peroxidation (LPX) and total hydroperoxides indicate the resultant oxidative stress in the Nosema exposed specimen. Increased superoxide dismutase (SOD) suggests activation of physiological mechanism to scavenge the superoxide radical produced during Nosema infection. Higher activities of catalase and glutathione-S-tranferase on $18^{th}$ d indicate adaptive behaviour of the tissue against oxyradicals. The results suggest that Nosema infection is involved in altering the active oxygen metabolism by modulating LPX and reactive oxygen species (ROS), which is indicative of pebrine disease disorder.