Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activities of serum creatine kinase (CK), lactate dehydrogenase (LD) and LD isoenzymes were studied in 14 Prestice black pied pigs from a herd affected with congenital tremor. Mean CK activity was 19.57 +/- 3.56 mu kat.l-1 for 6 adult pigs, and it was 21.03 +/- 1.33 mu kat.l-1 and 20.42 +/- 1.23 mu kat.l-1 for the affected (n = 5) and control (n = 3) piglets, respectively. No significant differences were demonstrable between the groups in CK activity. Total serum LD and LD-4 as well as LD-5 isoenzyme activities were higher in sows. Piglets affected with congenital tremor showed an increase in total LD enzyme and LD-5 isoenzyme activity. It is concluded that no relationship exists between congenital tremor and serum CK activity in piglets. At the same time, there is a positive relationship between congenital tremor and significantly (P < 0.01) elevated LD enzyme and LD-5 isoenzyme activity. The results allow us to suggest that total lactate dehydrogenase and LD-5 isoenzyme activities could be used as biological markers of congenital tremor in piglets.
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PMID:Activity of serum creatine kinase, lactate dehydrogenase and LD isoenzymes in piglets affected with congenital tremor: a case report. 130 96

Oxyrase is an enzyme mixture coveted by microbiologists for its unique ability to remove O2 from media in which anaerobic bacteria are grown. The study reported here examined the potential usefulness of Oxyrase as an adjunct to gassing freshly isolated rat proximal tubules (RPT) with 95% N2-5% CO2 in an attempt to achieve totally O2-free conditions (anoxia) before initiating studies on the mechanism of O2 deprivation injury in vitro. RPT, in 6 ml of Krebs-Henseleit buffer (KHB), were initially gassed with 95% N2-5% CO2 at 1.5 liters/min for 5 min and incubated for 15 to 30 min at 37 degrees C in a shaking water bath, pO2 decreased from approximately 400 to 80 mm Hg. If RPT were present in the KHB, pO2 was even lower, i.e., approximately 50 mm Hg. Addition of increasing concentrations of Oxyrase (300 to 1,500 mU) to KHB alone, that is, without RPT, reduced pO2 from 80 mm Hg to less than 5 mm Hg; increasing the gas rate from 1.5 to 3.0 liter/min of 95% N2-5% CO2, the concentration of Oxyrase to 1,800 mU, and adding RPT reduced pO2 to zero. In this latter condition, pO2 remained unmeasurable during the 20 min of study and neither pH nor pCO2 changed compared with control values. Oxyrase (1,800 mU) had no effect on lactate dehydrogenase release, a sign of membrane injury, in normoxic RPT in KHB. We conclude that anoxia can easily be achieved by the addition of Oxyrase to KHB in which RPT are suspended, if the appropriate concentration of Oxyrase is added and if the RPT are gassed with 95% N2-5% CO2. This concentration of Oxyrase exerts no detrimental effects on RPT gassed with 95% O2-5% CO2.
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PMID:A novel method of inducing and assuring total anoxia during in vitro studies of O2 deprivation injury. 213 35

Hepatocytes from isolated rat livers were hypothermically incubated (5 degrees C) in an oxygenated environment with continuous shaking (to simulate organ perfusion preservation). The incubation solution was either a tissue culture medium (L-15), an organ preservation perfusate (UW gluconate), or a simple cold-storage solution used for organ preservation (UW lactobionate). Hepatocyte viability was assessed from the release of lactate dehydrogenase (LDH) into the incubation medium. Cell swelling (due to the uptake of water) was also measured. Within 24 hr, hepatocytes hypothermically stored in each of the three incubation solutions became swollen (30 to 40% water gain) and lost a significant amount of LDH (as much as 60%). The addition of polyethylene glycol (PEG; relative molecular mass 8000; 5 g%) to the solutions suppressed cell swelling and allowed the incubated hepatocytes to remain relatively well preserved (30% LDH release) for as long as 120 hr. Adding either dextran (relative molecular mass 10,000 to 78,000; 5 g%) or saccharides (100 mmol/liter) instead of PEG neither prevented cell swelling nor prevented the cells from dying. The results of this study suggest (i) there is a direct correlation (r = 0.873) between hypothermia-induced cell swelling and cell death (i.e., the suppression of cell swelling prevents cell death); (ii) the mechanism by which PEG prevents cell swelling (and thus maintains cell viability) is not related to the osmotic or oncotic properties of the molecule but instead is apparently related to some unknown interaction between PEG and the cell, an interaction that provides stability during hypothermic incubation; and (iii) hypothermia-induced cell swelling must be prevented if isolated hepatocytes are to be used as a model for studying the mechanism by which cell damage occurs during hypothermic organ preservation. By eliminating cell death due to cell swelling, the biochemical mechanisms of cell death can be studied.
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PMID:Hypothermic preservation of hepatocytes. I. Role of cell swelling. 248 Aug 65

Benzyl chloride (BCl) is used in the manufacture of basic and acidic dyes, pharmaceutical products, resins, and synthetic tannins. BCl is known to have caused liver malfunctions in some workers exposed to 2 ppm BCl vapors. This study was conducted to investigate the effect of BCl on isolated male rat hepatocytes using several toxicity parameters. The hepatocytes were isolated by a collagenase perfusion technique and were incubated in airtight tubes with 1.8 and 3.6 mM BCl in a shaking water bath at 37 degrees C for 10, 30, 60, and 120 min. Throughout the incubation period the cell viability was determined by trypan blue exclusion and leakage of cytosolic enzymes such as lactate dehydrogenase (LDH), aspartate transaminase (AST), and alanine transaminase (ALT). Exposure to BCl resulted in a significant decrease in cell viability as assessed by trypan blue and significant increase in leakage of these enzymes compared to the controls.
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PMID:Effect of benzyl chloride on rat hepatocytes. 319 58

1. Isolated rat hepatocytes were exposed to the fumigant 1,2-dibromoethane (DBE) and cytotoxicity was evaluated by studying parameters of cellular function and lipid peroxidation. 2. DBE caused plasma membrane damage, as determined by leakage of lactate dehydrogenase, and was more severe in shaken suspensions than stationary suspensions, suggesting that cells were more fragile after DBE exposure. 3. DBE decreased hepatocyte glycogen content and stimulated albumin synthesis in hepatocyte suspensions. 4. Lipid peroxidation resulted from DBE exposure and was greater in cells isolated from phenobarbital-pretreated rats. Shaking the suspensions enhanced lipid peroxidation. Ethane production did not parallel formation of thiobarbituric acid reactants, suggesting that these parameters of lipid peroxidation reflect different mechanisms of molecular interaction of DBE.
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PMID:Effects of 1,2-dibromoethane on isolated hepatocytes: functional alterations and induction of lipid peroxidation. 342 Sep 45

Rat liver enzymes were used to study the relationship between their in vivo half-lives and their apparent hydrophobicity or their resistance to inactivation by mechanical shaking. The apparent hydrophobicity of these enzymes, measured as the percent of the protein recovered from an octyl-Sepharose column, is correlated with their known half-lives (r = 0.75, P less than 0.01). The presence of specific ligands which are known to increase compactness by impeding unfolding of proteins decreased the apparent hydrophobicity of fructose-1,6-bisphosphatase, glucose-6-phosphate dehydrogenase, glyceraldehyde-3-phosphate dehydrogenase, and pyruvate kinase. Resistance of enzymes to inactivation by mechanical shaking correlated well with their in vivo half-lives (r = 0.90, P less than 0.01). When the shaking experiments were done in the presence of substrates, fructose-1,6-bisphosphatase, glucose-6-phosphate dehydrogenase, glyceraldehyde-3-phosphate dehydrogenase and lactate dehydrogenase were protected from inactivation.
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PMID:Protein hydrophobicity and stability support the thermodynamic theory of protein degradation. 633 12

Thirty-four chemicals-diverse in structure, postulated mechanisms of action, and primary target organs--were tested for cytotoxic response in isolated hepatocyte suspensions from young male Sprague-Dawley rats. Hepatocytes were incubated in the presence and absence of the test chemicals in closed vessels fitted with side arms for serial sampling for up to 5 h at 37 degrees C with gentle shaking under an O2:CO2 (95:5) atmosphere. The parameters evaluated were glutamate-oxaloacetate transaminase and lactate dehydrogenase release from the cells, Trypan blue exclusion, cell count, urea synthesis capability, and steady-state ATP levels. All chemicals cytotoxic in animals following single or short-term repeated exposures caused statistically significant changes in one or more of these parameters in the 0.01-10-mM concentration range. Dimethylnitrosamine and thioacetamide were not as potent in the isolated cell system as expected from their in vivo hepatotoxicity, and the quantitative changes produced with thioacetamide in the hepatocytes were marginal, even at 10 mM. The solvents tested--ethanol, acetone, dimethyl sulfoxide (DMSO), and propylene glycol--were without effect. These results indicate that isolated hepatocyte suspensions are useful for the identification of cytotoxins in general and hepatotoxins in particular, but that their capability for yielding a quantitative index of cytotoxic potential for diverse chemical species remains to be demonstrated.
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PMID:Response of isolated hepatocytes to organic and inorganic cytotoxins. 662 Mar 99

We have previously shown that shaking the culture plates (SHAKE) of rabbit renal proximal tubule cells (RPTC) to maintain adequate aeration increased aerobic metabolism and decreased the induction of glycolysis compared to RPTC cultured under standard conditions (STILL). However, glycolysis in SHAKE RPTC remained elevated compared to glycolysis in proximal tubules in vivo. In the present study the contribution of culture medium sugar composition and concentration to glycolytic metabolism was assessed in RPTC. SHAKE and STILL RPTC cultured in 5 mM glucose contained lactate levels equivalent to the respective SHAKE and STILL RPTC cultured in standard culture medium which contains 17.5 mM glucose. Similarly, the activity of lactate dehydrogenase was unchanged by lowering the medium glucose concentration. Substituting 5 mM galactose for 5 mM glucose in the culture medium significantly reduced the lactate content of both SHAKE and STILL RPTC but had no effect on lactate dehydrogenase activity. Cell growth was equivalent under all culture conditions. Sensitivity to mitochondrial inhibition was determined for each culture condition by measuring cell death after exposure to the respiratory inhibitor antimycin A. The results showed a hierarchy of sensitivity to antimycin A (5 mM galactose SHAKE > 5 mM glucose SHAKE > 17.5 mM glucose SHAKE = 17.5 mM glucose STILL), which was generally inversely correlated with the level of glycolysis as measured by lactate content (17.5 mM glucose STILL > 17.5 mM glucose SHAKE = 5 mM glucose SHAKE > 5 mM galactose SHAKE).
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PMID:Decreasing glycolysis increases sensitivity to mitochondrial inhibition in primary cultures of renal proximal tubule cells. 819 71

This study examined the role of odd and even short-chain fatty acid substrates on aerobic and glycolytic metabolism in well-aerated primary cultures of rabbit renal proximal tubule cells (RPTC). Increasing oxygen delivery to primary cultures of RPTC by shaking the dishes (SHAKE) reduced total lactate levels and lactate dehydrogenase (LDH) activity and reduced net glucose consumption compared to RPTC cultured under standard conditions (STILL). The addition of butyrate, valerate, heptanoate, or octanoate to SHAKE RPTC produced variable effects on glycolytic metabolism. Although butyrate and heptanoate further reduced total lactate levels and net glucose consumption during short-term culture (< 24 h), no fatty acid tested further reduced total lactate levels, net glucose consumption, or LDH activity during long-term culture (7 days). During the first 12 h of culture, maintenance of aerobic metabolism in SHAKE RPTC was dependent on medium supplementation with fatty acid substrates (2 mM). However, by 24 h, SHAKE RPTC did not require fatty acid substrates to maintain levels of aerobic metabolism equivalent to freshly isolated proximal tubules and greater than STILL RPTC. This suggests that SHAKE RPTC undergo adaptive changes between 12 and 24 h of culture, which give RPTC the ability to utilize other substrates for mitochondrial oxidation, therefore allowing greater expression of mitochondrial oxidative potential in SHAKE RPTC than in STILL RPTC.
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PMID:The role of short chain fatty acid substrates in aerobic and glycolytic metabolism in primary cultures of renal proximal tubule cells. 837 17

Simple cold storage of livers for transplantation activates glycolysis due to lack of oxygen. Energy derived from glycolysis may be critical for cell survival and liver cell death may occur once glycolysis is inhibited in the liver due to accumulation of end products or lack of substrates (glycogen). The relationship between cell death (lactate dehydrogenase, LDH release), anaerobic glycolysis (lactate production), and glycogen content of liver tissue was studied during cold incubation of liver slices in UW solution. Rat livers slices from male Sprague Dawley rats were incubated at 4 degrees C in UW solution, with continuous gentle shaking, under conditions of chemical hypoxia (KCN, 5 mM). The rate of lactate production, LDH release-ATP and glycogen content were measured spectrophotometrically and by HPLC. Lactate increased nearly linearly for the first 48 h of incubation; total lactate which had accumulated after 48 h was 33.9 +/- 0.81 mumol/g and at 96 h nearly the same, 31.3 +/- 1.2 mumol/g. Glycolysis stopped, apparently, because of the depletion of liver slice glycogen which was initially 228.8 +/- 1.7 mumol/g wet wt. It decreased to 34.7 +/- 2.7 mumol/g at 48 h and to 18.7 +/- 1.1 mumol/g at 72 h and remained at this level for the next 24 h. An increased leakage of LDH occurred once glycogen metabolism (and accumulation) ceased. LDH release could be stimulated after only a few hours of cold incubation of liver tissue slices by adding glycolysis inhibitor (iodoacetic acid) to the medium. After 24 h. LDH release was 24.4 +/- 1.8% and increased to 52.8 +/- 5.2% (P < 0.05, Student's t-text) with iodoacetic acid. Adding a glycolytic substrate (fructose, 10 mM) to the medium maintained lactate production for 96 h. The stimulation of glycolysis by fructose also reduced cell death: LDH release was significantly lower at 72- and 96-h incubation (P < 0.001, two-way ANOVA). The ATP content was significantly higher with fructose (P < 0.001). Adding glucose (20 mM) and fructose (10 mM) in combination resulted in prolonged cell survival, significantly delayed glycogen depletion and significantly higher ATP content at 48 and 72 h (two-way ANOVA). Livers from rats who had fasted for 24 h demonstrated the same LDH release at 48 h when incubated with glucose (20 mM) and fructose (10 mM). In conclusion, LDH leakage from hypoxic cold-stored liver slices is related to anaerobic glycolysis. Anaerobic glycolysis appears to continue slowly under hypothermia and provides sufficient energy for maintenance of cell viability. A stimulation of glycolysis in the cold is possible by fructose and results in prolonged cell survival under hypothermic conditions. Glycogen depletion can be slowed down by combining glucose and fructose.
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PMID:[Liver metabolism during cold ischemic incubation in UW solution in the rat model]. 949 7


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