• Journal of the Korean Society of Food Science and Nutrition
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• v.20 no.5
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• pp.409-417
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• 1991

To investigate effects of chronic alcohol consumption and tocopherol on lipid peroxidation and mitochondrial respiration 48 male rats of Sprague-Dawley strain were divided into 4 groups. Each group received for 3 weeks one of 4 experimental diets: tocopherol deficient control (TDC), tocopherol deficient-ethanol (TDE), tocopherol-supplemented control (TSC) and tocopherol-supplemented-ethanol (TSE). Composition of the diets was based on the Lieber and Decarli liquid diet and $\alpha$-tocopherol was supplemented at the level of 30mg/liter of diet, and ethanol supplied 36kcal%. TDC and TSC were pair-fed to TDE and TSE, respectively. Increase of body weight of tocopherol deficient-ethanol group was the lowest and the effect was diminished with tocopherol supplementation. Respiration of liver mitochondria was depressed in ethanol-administered groups and the effect became larger with tocopherol deficiency. Hepatic lipid peroxide level was not influenced by ethanol, but hepatic tocopherol content decreased with ethanol treatment. The result indicated that, although lipid perroxide level was unchanged with chronic ethanol consumption, oxidative stress exists in tissues of rate administered ethanol and may be relieved by tocopherol supplementation.

• Toxicological Research
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• v.5 no.1
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• pp.27-35
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• 1989

When acetaminophen (25mM) was introduced into the perfused rat liver, the hepatic O2 uptake was rapidly inhibited first and then later slow-down. The rapid inhibition was found to be due to mitochondrial blockade, whereas the so-called slow inhibition" was associated with microcirulatory aberrations as evidenced by inhomogneous staining of the liver tissue by trypan blue infusion (0.1%). NaCN (0.5mM) also caused rapid and slow respiratory inhibitions, giving heterogeneous trypan blue staining.ning.

• Journal of Nutrition and Health
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• v.17 no.4
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• pp.297-304
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• 1984

The effect of dietary fish oil ( mackerel oil : MO, eel oil : EO) on energy utilization in rats was studied with measurements of various tissue lipoprotein lipase( LPL ) and live and heart mitochondrial respiration. Fatty acid composition of mitrochondrial inner membrane matrix was also investigated. Dietary fat level was 10%( w/w) and reference groups were fed soybean oil (SO), repeseed oil ( RO) and beef tallow( BT ). Activity of LPL was about 60% higher in post-heparin plasma and 2 to 3 times higher in adipose tissue of BT group than fish oil or vegetable oil group. But there was no significant difference between fish oil and vegetable oil groups. Inclusion of EO above 2% (w/w) in dietary fat with fille oil of BT, markedly reduced both post -heparin plasma and adipose tissue LPL. Effects of MO and EO were not different in adipose tissue LPL, but EO was more effective than MO, in reducing post -heparin plasma LPL when mixed fat with varying amount of fish oil was used. Hepatic mitochondria isolated from fish oil-fed group showed the lowest rate of respiration but had P/O ratio comparable to SO and BT groups. On the other hand, cardiac mitochondria of fish oil group showed no difference in all the mitochondrial respiration parameters observed RO group had lowest P/O ratio both in hepatic and cardiac mitochondria. Fatty acid compositions of mitochondrial lipid differ between SO, RO, BT and MO groups, notably in the content of $C_{22:1}$ fatty acid.

• Journal of Community Nutrition
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• v.7 no.3
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• pp.163-168
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• 2005

The present investigation was undertaken in vivo to determine whether the functional alterations of hepatic mitochondria induced by ethanol might be prevented by taurine. We examined the effects of supplementation of taurine on hepatic mitochondrial oxidative phosphorylation in the chronic ethanol-administered rats. Isolated hepatic mitochondria from three groups of rats were functionally tested by an analysis of $\beta-hydroxbutyrate-supported$ respiration and the coupling of this process to ATP synthesis in the presence of ADP. The three groups were control group(CO), ethanol(60g/L) administered group (AL), and ethanol (60g/L) + taurine (5g/L) supplemented group (AT). Ethanol and/or taurine were given in drinking water for 10 weeks. The mitochondria from AL group had lower state 4 respiratory rate, respiratory control (RC) ratio and ADP : O(P/O) ratio than those from CO and AT group. It showed that the ethanol administered rats were less coupled and thus less efficient with respect to mitochondrial ATP synthesis than both control rats and ethanol + taurine supplemented rats. It suggests that taurine supplementation might improve the impaired oxidative phosphorylation efficiency in mitochondrial dysfunction that is recognized as a cause of liver diseases in chronic ethanol consumption.

• Journal of Nutrition and Health
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• v.20 no.6
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• pp.432-441
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• 1987

This study was undertaken to investigate effects of alcohol and fat content in a balanced diet on growth, hepatic function and some biochemical indices of blood in growing rats. Fourty eight male rats of Sprague-Dawley strain weighing about 160g were divided into 4 groups ; high fat diet group, alcohol-adminstered high fat diet group, low fat diet group and alcohol-administered low fat diet group. High and low fat diet supplied 30% and 12%, respectively, of total calorie intake from fat and alcohol-treated groups received water containing 10% ethanol. Diets contained adequate amounts of all nutrients required for rats, including lipotropic agents(choline and methionine) to minimize effects of factors other than alcohol on liver function. Growth rate was lowest in alcohol-administered low-fat diet group, despite that their energy intake was equivalent to the others. For a 3-week study period, 21.86% and 23.61% of total calorie intake were derived from alcohol in alcohol-adminitered high fat diet group and low fat diet group, respectively. There was no influenced on vitamin B$_1$ status by alcohol consumption. Concentration of triglyceride in plasma increased with alcohol comsumption, and the effect was greater after 6 weeks than after 3 weeks of alcohol consumption . Difference of dietary fat content did not affect the level of triglyceride . The levels of total cholesterol and HDL-cholesterol in plasma were not influenced by alcohol consumption. Serum glutamate pyruvate transaminase activity and hepatic mitochondrial respiration rate did not differ between groups. The results indicate that neither moderate alcohol drinking for 6 weeks nor fat content with a balanced diet caused any dramatic change of metabolism and liver function in rats. However they suggest that even moderate alcohol consumption can affect growth of animals dramatically and the effect may be lessened with relatively high fat content in diet.

• Preventive Nutrition and Food Science
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• v.5 no.4
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• pp.230-233
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• 2000

The present work was designed to determine whether change in fluidity of the mitochondrial membrane affects mitochondrial {TEX}$F_{1}${/TEX}{TEX}$F_{0}${/TEX}ATPase characteristics in NIDDM-prone BHE/Cdb rat. Isolated mitochondria fom BHE/Cdb rat fed a 6% coconut oil or corn oil were functionally tested by an analysis of its respiration and the coupling of this process to ATP synthesis in presence of oligomycin, a specific inhibitor of oxidative phosphorylation (OXPHOS), that binds to the {TEX}$F_{1}${/TEX}{TEX}$F_{0}${/TEX}ATPase. Mitochondria from rats fed coconut oil were more responsive to the inhibitory action of oligomycin with respect to state 3 respiration, respiratory control (RC) ratio and ADP:P (P/O) ratio than were mitochondria from rats fed corn oil. In state 3 respiration, mitochondria from rats fed coconut oil consumed less oxygen than did mitochondria from rats fed corn oil. RC ratio was lower in the mitochondria from rats fed coconut oil than was mitochondria from rats fed corn oil. In P/O ratio, the mitochondria from rats fed coconut oil had a lower P/O ratio than did mitochondria from rats fed corn oil. The data showed that the chang influidity of the mitochondrial membrane by dietary fat affected mitochondrial {TEX}$F_{1}${/TEX}{TEX}$F_{0}${/TEX}ATPase characteristics. The present study on diet differences in {TEX}$F_{1}${/TEX}{TEX}$F_{0}${/TEX}ATPase characteristics provides considerable insight into the role diets play in the control of mitochondrial function, expecially OXPHOS in NIDDM with mitochondrial defects.

• Journal of the Korean Society of Food Science and Nutrition
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• v.14 no.2
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• pp.145-150
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• 1985

This study was conducted to examine the pharmacological effect of water soluble extract of Lichens (Parmelia, Physcia and Cladonia species) on liver-damaged rat by $CCl_4$ injection. Rat livers were damaged acutely and chronically by one-time injection of $CCl_4$ just prior to five days of experimental period and continuous injections in every three days for eight weeks of experimental period, respectively. During each period the experimental group was fed Lichens extract(5.5 mg of dry wt/ml) instead of water given to the control group. For both acute and chronic liver damage, the experimental group showed higher oxidative activity of hepatic mitochondria measured by state 3 respiration, P/O ratio, respiratory control and ATP synthesized, compard to the control group. Serum glucose was slightly higher in the experimental group but liver glycogen showed no significant difference between experimental and control groups. In experimental group, liver glucose-6-phosphatase activity was increased during first two days after acute liver damage, but not significantly different from control group during chronic damage. Liver lactate, malate plus fumarte and glutamate tended to be higher in the experimental group, especially for chronic liver damaged rat. It is concluded that Lichens extract stimulate cytoplasmic and mitochondrial oxidative activities and the possible mechanism of the latter is supposed to involve the preservation of membrane integrity by certain component(s) of water-soluble Lichens extract.

• Journal of The Korean Society of Clinical Toxicology
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• v.2 no.1
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• pp.54-57
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• 2004

Disulfiram (tetraethylthiuram disulphid) is used in the treatment of chronic alcoholism since it causes an unpleasant aversive reaction to alcohol. It works by inactivating hepatic aldehyde dehydrogenase, leading to pronounced rise in the acetaldehyde concentration when ethanol is metabolized. Acetaldehyde causes alcohol sensitivity, which involve vasodilation associated with feeling of hotness and facial flushing, increased heart rate and respiration rates, lowered blood pressure, nausea, headache. One of its metabolites, diethyldithiocarbamate (DDC) can inhibit the enzyme dopamine $\beta$-hydroxylase (DBH), this may account for the profound refractory hypotension and hypothermia seen with the disulfiram-ethanol reaction (DER), resulting from norepinephrine depletion. This report is presents the case of a patient we met, who presented with hypothermia caused by the disulfiram-ethanol reaction, and along with a brief review of the subject.

• Journal of Korean Academy of Nursing
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• v.13 no.2
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• pp.87-104
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• 1983

It has been well documented that animals exposed to cold show increased activity of thyroid gland. The calorigenic action of thyroid hormone has been demonstrated by a variety of in vivo and in vitro studies. According to Edelman et al., the thyroid thermogenesis is due to activation of energy consuming processes, especially the active sodium transport by the hormone in target tissues. If so, the increase in thyroid activity during cold exposure should induce increased capacity of sodium transport in target tissue and the change in tissue metabolism should be precisely correlated with the change in Na+_K+_ATPase activity of the tissue. This possibility was tested in the present study: in one series, changes in oxygen consumption and Na+_K+_-ATPase activity of liver preparations were measured in rats as a function of thyroid status, in order to establish the effect of thyroid hormone on the tissue respiration and enzyme system in another series, the effect of cold stimulus on the serum thyroid hormone level, hepatic tissue oxygen consumption and Na+_K+_ATPase activity in rats. The results obtained are as follows: 1. The Na+_dependent oxygen consumption of liver slices, the oxygen consumption of liver mitochondria and the Na+_K+_ATPase activity of liver preparations were significantly inhibited in hypothyroidism and activated in hyperthyroidism. Kinetic analysis indicated that the Vmax. of Na+_K+_ATPase was decreased in hypothyroidism and increased in hyperth)'roidism. 2. In cold exposed rats, the serum triiodothyronine (T₃) level increased rapidly during the initial one day of cold exposure, then declined slowly to the control level after two weeks. The serum thyroxine (T₄) level decreased gradually throughout the cold exposure. Accordingly the T₃/T₄ratio increased. The mitochondrial oxygen consumption and the Na+_dependent oxygen consumption of liver slices increased during the first two days and then remained unchanged thereafter The activity of the Na+_K+_ATPase in liver preparations increased during cold exposure with a time course similar to that of oxygen consumption. Kinetic analysis indicated that the Vmax. of Na+_K+_ATPase increased. 3. Once the animal was adapted to cold, induction of hypothyroidism did not significantly alter the hepatic oxygen consumption and Na+_K+_ATPase activity. These results indicate that: 1) thyroid hormone increases capacities of mitochondrial respiration and active sodium transport in target tissues such as liver; 2) the increased T₃level during the initial period of cold exposure facilitates biosynthesis of Na+_K+_ATPase and mitochondrial enzymes for oxidative phosphorylation, leading to enhanced production and utilization of ATP, hence heat production.

• Asian-Australasian Journal of Animal Sciences
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• v.24 no.6
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• pp.857-866
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• 2011

This study examined the metabolism of free radicals in hepatic mitochondria of goats induced by lipopolysaccharide (LPS), and investigated the effects of melatonin (MT). Forty-eight healthy goats ($10{\pm}1.2\;kg$) were randomly selected and divided into four groups: saline control, LPS, MT+LPS and MT. The goats within each group were3 sacrificed either 3 or 6 h after treatment and the livers removed to isolate mitochondria. The respiration control ratio (RCR), the ADP:O ratio, the oxidative phosphorylation ratio (OPR), the concentration of $H_2O_2$ and the activities of Complex I-IV were determined. The mitochondrial membrane potential ($\Delta\psi_m$) was analyzed by flow cytometry. The results showed that RCR, O/P and OPR of the LPS group decreased (p<0.05), as well as activities of respiratory complexes, whereas the generation of $H_2O_2$ in Complex III increased (p<0.05) after 3 h, while Complex II and III increased after 6 h. Also, it was found that the mitochondrial membrane potential of the LPS group declined (p<0.05). However, pre-treatment with MT attenuated the injury induced by LPS, which not only presented higher (p<0.05) RCR, O/P, OPR, and respiratory complex activities, but also maintained the $\Delta\psi_m$. Interestingly, it is revealed that, in the MT+LPS group, the generation of $H_2O_2$ increased firstly in 3 h, and then significantly (p<0.05).decreased after 6 h. In the MT group, the function of mitochondria, the transmenbrane potential and the generation of $H_2O_2$ were obviously improved compared to the control group. Conclusion: melatonin prevents damage caused by LPS on hepatic mitochondria of goats.