不同季节高原鼢鼠乳酸脱氢酶活力和同工酶谱

目的:探讨高原鼢鼠对洞道低氧高二氧化碳环境的代谢适应机制。方法:用酶活力分析法,分析春季、夏季和秋季高原鼢鼠血清乳酸脱氢酶(LDH)活力、乳酸含量和组织LDH活力,用聚丙烯酰胺凝胶电泳法分析血清和组织LDH同工酶谱。结果:高原鼢鼠血清LDH活力在春夏秋三季具有明显的差异,春季高于夏季,夏季高于秋季,血清乳酸含量表现出同样的变化趋势;春季血清中五种同工酶条带都清晰可见,夏季血清中LDH5和LDH4清晰可见,秋季血清中只能看见LDH5带。骨骼肌、心肌和脑组织LDH活力较高,而且从春季到秋季显著降低;肝、肾和肺组织LDH活力较低,肝组织LDH活力春季显著高于夏季和秋季,夏秋两季之间没有明显差异;肾和肺组织LDH活力在春季与夏季之间没有明显差异,但秋季明显降低。心、肝、肺、肾、脑和肌肉组织LDH同工酶谱,在春夏秋三季都显示出五条带,并表现出明显的组织差异;各组织同工酶含量也有不同程度的季节差异。结论:高原鼢鼠体内糖酵解过程具有明显的季节性变化,从春季到秋季依次降低,这与它们的季节性活动特点和洞道中氧气和二氧化碳的季节性波动有关。     

Alterations in glycolytic and oxidative potentials of rat brain during acute and chronic acephate treatments

Alterations in the rat brain carbohydrate and related metabolisms were studied during acute and chronic acephate toxicity. The rats were divided into three batches of eight in each batch. The first batch was treated with chronic (50 mg.Kg-1.day-1 for 7 weeks) and second batch was treated with acute (600 mg.Kg-1.day-1 for one day) doses of acephate, third group was served as control which received vehicle only. The representative enzymes like SDH, MDH, LDH, GDH, AAT and AlAT activities were decreased significantly during chronic treatment. Whereas MDH, LDH, AAT and AlAT activities showed significant increase during acute treatment. The glycogen and pyruvate levels showed nonsignificant elevation and lactate and total carbohydrate levels were depleted in the brains of chronic acephate treated rats. Reverse trend was observed with regard to lactate and pyruvate during acute toxicity whereas the total carbohydrates and glycogen levels were significantly elevated. The decreased oxidative potential and reduced flux of ketoacids into TCA cycle through transamination reactions indicate that acephate caused energy crisis in the brain during chronic treatment. During acute treatment the inhibited succinate oxidation was compensated by the ketoacid contributions through transamination reactions. The neuro transmitter balance with particular reference to glutamate during toxic stress was reflected through the GDH levels in both the treatments.     

Effect of whole body gamma radiation on hepatic LDH activity,lactate, pyruvate concentration and rate of oxygen consumption in Bufo melanostictus

Whole body Co60 gamma radiation induced changes in lactic dehydrogenase (LDH) activity, pyruvate, lactate content and rate of oxygen (O2) consumption in a tropical hibernating anuran (Bufo melanostictus). In 3.5 and 7 Gy treated groups, a significant increase in LDH activity and lactate/pyruvate ratio was observed, whereas a significant decrease in O2 consumption rate was observed in treated animals on post-irradiation day (PID) 1, 5 and 10. Increase in LDH activity was observed on PID-1 in both the treated groups, reached to a peak on PID-5 in 7 Gy treated group and then declined on PID-10.     

Studies on the ameliorative effect of curcumin on carbofuran induced perturbations in the activity of lactate dehydrogenase in wistar rats

Carbofuran is known to inhibit neurotransmission system of insects. The present study was undertaken to evaluate the possible ameliorative effect of curcumin on carbofuran induced alterations in energy metabolism in brain and liver of rats. The results demonstrate that carbofuran caused a significant inhibition of lactate dehydrogenase (LDH) activity in rat liver but an increase in LDH activity in the brain. Increased LDH activity was also observed in the serum indicating organ damage in treated animals. Carbofuran caused an increase in level of pyruvic acid in rat liver but a decrease in the brain. A decrease in the level of soluble protein was also observed in the tissues studied. Pretreatment of animals with curcumin resulted in significant amelioration of the altered indices. These results indicate that carbofuran at sub lethal concentrations may adversely alter energy metabolism in brain and liver of non-target mammalian systems. Pretreatment of animals with curcumin may exhibit a potential to mitigate the carbofuran induced toxicity.     

The protective action of melatonin on indomethacin-induced gastric and testicular oxidative stress in rats

Reactive oxygen species and lipid peroxidation play a role in the pathogenesis induced by the non-steroidal anti-inflammatory drug indomethacin. Melatonin (MLT) protection against indomethacin-induced oxidative tissue injury was investigated in gastric mucosa and testis of rats. MLT was administered intragastrically (i.g.) 30 min before the administration to fasted rats of 20 mg indomethacin/kg rat given i.g.. The area of gastric lesion as well as thiobarbituric acid reactive substances (TBARS) and lactate dehydrogenase (LDH) activity were found to be significantly increased 4 h after administration of indomethacin in rat gastric mucosa and testis indicating acute oxidative injury. MLT pretreatment reduced gastric lesion area to 80% of the indomethacin-treated rats and reduced the rise in TBARS concentration. MLT treatment reduced the LDH activity increase in testis but not in gastric mucosa. In indomethacin-treated rats, both the cytosolic Cu,Zn superoxide dismutase (Cu,Zn-SOD) and mitochondrial Mn-SOD activities were significantly diminished in gastric mucosa as well as the total SOD activity in testis. In addition, glutathione (GSH) content in both tissues was markedly decreased following indomethacin treatment. Pretreatment with MLT significantly ameliorated both the inhibition of SOD activity and the decreased GSH content in both tissues. Thus, these results show the effective antiperoxidative and preventive actions of MLT against indomethacin-induced gastric mucosal damage and testicular oxidative injury and we propose that this action might be relevant for its use with other free radical generating drugs.     

The effect of diabetes and insulin on adipose lactate dehydrogenase isozymes.

Adipose lactate dehydrogenase (LDH) (EC 1.1.1.27) isozyme distribution was altered in streptozotocin-diabetic and fasting rats resulting from a relative reduction of subunit A. Treatment with insulin for 2 days partially restored the relative content of isozyme 5 to control values in the diabetic rats, and the effect of insulin was not inhibited by simultaneous injection of actinomycin D or puromycin. When the epididymal adipose tissues isolated from control animals were incubated in vitro with dibutyryl adenosine 3',5'-cyclic monophosphate or epinephrine, a relative decrease in subunit A was observed; whereas, either compound caused an increase in subunit A in diabetic tissues. The findings suggest that the redistribution of LDH isozyme under these conditions is to prevent excessive accumulation of lactate in the tissue.     

Attenuation of the acute adriamycin-induced cardiac and hepatic oxidative toxicity by N-(2-mercaptopropionyl) glycine in rats

The protective effect of the synthetic aminothiol, N-(2-mercaptopropionyl) glycine (MPG) on adriamycin (ADR) induced acute cardiac and hepatic oxidative toxicity was evaluated in rats. ADR toxicity, induced by a single intraperitoneal injection (15 mg/kg), was indicated by an elevation in the level of serum glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT), creatine kinase isoenzyme (CK-MB), and lactic dehydrogenase (LDH). ADR produced significant elevation in thiobarbituric acid reactive substances (TBARS), indicating lipid peroxidation, and significantly inhibited the activity of superoxide dismutase (SOD) in heart and liver tissues. In contrast, a single injection of ADR did not affect the cardiac or hepatic glutathione (GSH) content and cardiac catalase (CAT) activity but elevated hepatic CAT. Pretreatment with MPG, (2.5 mg/kg) intragastrically, significantly reduced TBARS concentration in both heart and liver and ameliorated the inhibition of cardiac and hepatic SOD activity. In addition, MPG significantly decreased the serum level of GOT, GPT, CK-MB, and LDH of ADR treated rats. These results suggest that MPG exhibited antioxidative potentials that may protect heart and liver against ADR-induced acute oxidative toxicity. This protective effect might be mediated, at least in part, by the high redox potential of sulfhydryl groups that limit the activity of free radicals generated by ADR.     

瑞氏七鳃鳗乳酸脱氢酶（LDH）同工酶凝胶电泳分析

本文用聚丙烯酰胺凝胶电泳方法,对瑞氏七鳃鳗五种不同组织（骨骼肌、心、肾、肠、鳃）中ＬＤＨ同工酶进行了分析研究,结果表明,ＬＤＨ同工酶具有组织特异性,其中骨骼肌中含有五种ＬＤＨ同。酶,即ＬＤＨ１、ＬＤＨ２、ＬＤＨ３、ＬＤＨ４、ＬＤＨ５,鳃含有ＬＤＨ１和ＬＤＨ４而肾和心只含有ＬＤＨ１,肠只含有ＬＤＨ４。     

Attenuation of the acute adriamycin-induced cardiac and hepatic oxidative toxicity by N-(2-mercaptopropionyl) glycine in rats

The protective effect of the synthetic aminothiol, N-(2-mercaptopropionyl) glycine (MPG) on adriamycin (ADR) induced acute cardiac and hepatic oxidative toxicity was evaluated in rats. ADR toxicity, induced by a single intraperitoneal injection (15 mg/kg), was indicated by an elevation in the level of serum glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT), creatine kinase isoenzyme (CK-MB), and lactic dehydrogenase (LDH). ADR produced significant elevation in thiobarbituric acid reactive substances (TBARS), indicating lipid peroxidation, and significantly inhibited the activity of superoxide dismutase (SOD) in heart and liver tissues. In contrast, a single injection of ADR did not affect the cardiac or hepatic glutathione (GSH) content and cardiac catalase (CAT) activity but elevated hepatic CAT. Pretreatment with MPG, (2.5 mg/kg) intragastrically, significantly reduced TBARS concentration in both heart and liver and ameliorated the inhibition of cardiac and hepatic SOD activity. In addition, MPG significantly decreased the serum level of GOT, GPT, CK-MB, and LDH of ADR treated rats. These results suggest that MPG exhibited antioxidative potentials that may protect heart and liver against ADR-induced acute oxidative toxicity. This protective effect might be mediated, at least in part, by the high redox potential of sulfhydryl groups that limit the activity of free radicals generated by ADR.     

Effects of acepromazine on capture stress in roe deer (Capreolus capreolus)

The aim of this study was to evaluate effect of a short-acting neuroleptic (acepromazine) on capture stress response in roe deer (Capreolus capreolus). Sixteen roe deer were captured by drive-nets in the winters of 1998, 1999, and 2001. Roe deer were divided into two groups: animals in the treatment group received an intramuscular injection of acepromazine (0.093 mg/kg +/- 0.003 SEM; n = 8) while animals in the control group (n = 8) did not receive tranquilizer. Heart rate and body temperature, as well as hematologic and biochemical indicators of stress, were used to evaluate effect of the neuroleptic over 3 hr. Heart rate decreased over time after capture in both groups (P < 0.05), but stabilized sooner in the treated roe deer (75 min after capture) than in the controls (105 min after capture). Body temperature decreased over 45 min and then stabilized in both groups (P < 0.05). Comparisons of blood parameters revealed significantly lower red blood cell count (RBC), lymphocyte count, hemoglobin concentration, packed cell volume (PCV), and serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatine kinase (CK), and lactate dehydrogenase (LDH) activities in tranquilized animals compared with controls (at least P < 0.05). A reduction in PCV, lymphocyte count, and serum cortisol concentrations (at least P < 0.05) and an increase in serum creatinine levels (P < 0.05) were recorded over time in control animals, while a reduction in RBC and hemoglobin concentration (at least P < 0.05) and an increase in serum urea concentrations (P < 0.05) over time were observed in the treated group. Finally, a decrease in serum lactate and potassium levels and an increase in CK, AST, ALT, and LDH activities were recorded over time in both groups. Results obtained showed the suitability of using acepromazine in capture operations in order to reduce stress response and prevent its adverse effects in roe deer. The beneficial effect was not only due to the sedative effect of acepromazine, but also to peripheral vasodilatation.     

Arterial LDH, 2,3-DPG, lactate, pyruvate and acid-base balance in hypoxic albino rats of first or second generation

Arterial acid-base balance, lactate, pyruvate, lactate dehydrogenase activity (LDH), 2,3-diphosphoglycerate content (2,3-DPG) of normoxic control rats were compared with those of rats exposed to a hypoxic normobaric environment (10% O2 in N2) within a few hours after birth (hypoxic animals of first generation or H1), and with those of rats of second generation (H2) conceived and born in the above mentioned hypoxic environment of H1 parents and maintained always in the same place since their utilization. The H1 rats showed a displacement of acid-base balance towards acidosis and an increase of lactate, pyruvate, LDH and 2,3-DPG in comparison with normoxic controls. The H2 rats showed a significant attenuation of acidosis in comparison with H1 rats; the values of lactate, pyruvate, LDH and 2,3-DPG were intermediate between those found in H1 and normoxic control rats. We believe that these results are in relation with the evolution of adaptative processes to hypoxic environment in hypoxic animals of second generation.     

Different activity of glyoxalase system enzymes in specimens of Sparus auratus exposed to sublethal copper concentrations

The present study regards possible changes in the activity of glyoxalase system enzymes (glyoxalase I, GI, and glyoxalase II, GII) in tissues (brain, liver and white muscle) of the mediterranean bony fish Sparus auratus after a 20 days exposure to sublethal concentrations (0.1 or 0.5 ppm) of Cu in the marine water and on control untreated animals. The experiments also included measurements of copper concentration in the tissues, as well as of lactate dehydrogenase (LDH) activity, to evaluate possible Cu accumulation and changes in glycolytic activity respectively. Cu accumulation only occurs in the liver. GI, GII and LDH activities kept unchanged in the brain after copper exposure. GI activity in liver and muscle of copper-exposed animals decreases probably for a slackening in the glycolytic rate, as suggested by the lowering of LDH activity. GII activity remains unchanged or increases (liver extract, 0.5 ppm of Cu), maybe to safeguard enough cellular levels of GSH.     

Der Einfluß der Wurzelanaerobiose auf Äthanol-, Laktat- und Glukosegehalte sowie auf die Aktivitäten von ADH und LDH in Weizenkeimpflanzen

The effect of anaerobiosis of wheat seedling roots during 6 consecutive days on contents of ethanol, lactate and glucose in roots and shoots and on the exudation of ethanol from roots to the medium was examined. Activities of alcohol dehydrogenase (ADH) and lactate dehydrogenase (LDH) were determined. After 36 h of anaerobiosis the concentration of ethanol in roots increased temporarily about 6 times and after 6 days it decreased to the level of control plants. The exudation of ethanol from roots to the medium showed similar pattern. The content of lactate was unaffected by anaerobiosis. In contrast, the content of glucose in roots of seedlings increased already after 1 day of anaerobiosis about 2 times and this higher level of glucose was noticed during consecutive 5 days. Anaerobiosis of roots caused an increase in the activity of ADH in both roots and shoots but the increase was not related to the content of ethanol in tissues, or exudated to the medium. The activity of LDH was unaffected by this factor. The results are discussed in relation to the limitation of energy supply of plants grown under root anaerobiosis.     

Changes in MCT 1, MCT 4, and LDH expression are tissue specific in rats after long-term hypobaric hypoxia.

Little is known about the effect of chronic hypobaric hypoxia on the enzymes and transporters involved in lactate metabolism. We looked at the protein expression of monocarboxylate transporters MCT 1, MCT 2, and MCT 4, along with total lactate dehydrogenase (LDH) and LDH isozymes in skeletal muscle, cardiac muscle, and liver. Expression of these components of the lactate shuttle affects the ability to transport and oxidize lactate. We hypothesized that the expression of MCTs and LDH would increase after acclimation to high altitude (HA). The response to acclimation to HA was, however, tissue specific. In addition, the response was different in whole muscle (Mu) and mitochondria-enriched (Mi) fractions. Heart, soleus, and plantaris muscles showed the greatest response to HA. Acclimation resulted in a 34% increase in MCT 4 in heart and a decrease in MCT 1 (-47%) and MCT 4 (-47%) in plantaris Mu. In Mi fractions, the heart had an increase (+40%) and soleus a decrease (-40%) in LDH. HA also had a significant effect on the LDH isozyme composition of both the Mu and Mi fractions. Mitochondrial density was decreased in both the soleus (-17%) and plantaris (-44%) as a result of chronic hypoxia. We conclude that chronic hypoxia had a tissue-specific effect on MCTs and LDH (that form the lactate shuttle) but did not produce a consistent increase in these components in all tissues.     

Activity of Lactate Dehydrogenase in Serum and Cerebral Cortex of Immature and Mature Rats after Hypobaric Hypoxia

In our previous studies we have found both an increase of lipid peroxidation damage (expressed as levels of thiobarbituric acid-reactive substances) in brain and plasma lactate concentration in 21-day-old rats after a 30-min exposure to hypobaric hypoxia. Pretreatment of rats with l-carnitine decreased both parameters. The aim of our present study was to determine if the l-carnitine-dependent decrease of plasma lactate could be due to a modification of lactate dehydrogenase (LDH) activity. We followed brain and blood serum LDH activity of 14-, 21- and 90-day-old Wistar rats. We found an increase of brain LDH activity with age. However, we did not observe any significant differences in LDH activity after exposure to hypobaric hypoxia or l-carnitine pretreatment. In contrast to brain, serum LDH activity did not show any clear age-dependence. The hypoxia exposure increased LDH activity of 21-day-old rats only. Pretreatment of rats with l-carnitine decreased serum LDH activity of 21- and 90-day-old rats probably due to membrane stabilizing role of l-carnitine. In conclusions, acute hypobaric hypoxia and/or l-carnitine pretreatment modified serum but not brain LDH activity.     

高密度脂蛋白减轻小鼠内毒素性急性肺损伤

高密度脂蛋白(high density lipoprotein, HDL)是一种血浆含量丰富的脂蛋白,通常认为它可在体内发挥抗炎作用,能够与内毒素结合而抑制其生物活性.为探讨人HDL对内毒素性急性肺损伤的影响,将昆明小鼠分为假手术对照组、脂多糖(lipopolysaccharide, LPS)组、HDL组和LPS HDL组,腹腔注射LPS(10mg/kg体重)复制内毒素性急性肺损伤模型,于腹腔注射LPS 30min后经尾静脉给予人血浆HDL(70mg/kg体重),6h后结束实验.处死动物前抽取动脉血测定血气变化(PaO2, pH, PaCO2).处死后行支气管肺泡灌洗,计数灌洗液中白细胞(white blood cell, WBC)数量,测定蛋白含量和乳酸脱氢酶(lactate dehydrogenase, LDH)活性,并取肺组织进行病理学观察,测定肺组织湿/干重比值、丙二醛(malondialdehyde, MDA)含量、髓过氧化酶(myeloperoxidase, MPO)活性和肿瘤坏死因子-α(tumor necrosis factor α, TNF-α)含量.结果显示:(1)HDL改善小鼠肺换气功能,显著降低LPS所致的PaO2、pH的降低和PaCO2的增高(P<0.01);(2)HDL显著抑制LPS所致的肺泡灌洗液中WBC数量、总蛋白浓度和LDH活性的增高(P<0.01),降低肺组织湿/干重比值、MPO活性、MDA和TNF-α含量(P<0.05, P<0.01);(3)病理形态学分析及评分显示,HDL治疗组小鼠在出血、肺水肿及肺组织内中性粒细胞浸润的程度均低于LPS所致肺损伤组(P<0.01).结果提示,HDL可减轻小鼠内毒素性急性肺损伤.     

Lactate dehydrogenase activity of rat epididymis and spermatozoa: effect of constant light

During its passage through the epididymis, the gamete undergoes a process of "maturation" leading to the acquisition of its fertilizing ability. The epididymis displays regional variations in the morphology and metabolic properties of its epithelium which are relevant for the progressive development of mature sperm characteristics. The epididymis has spontaneous peristaltic contractions and receives sympathetic innervation that is modulated by melatonin, a hormone synthesized and released by the pineal gland. Constant lighting disrupts melatonin synthesis and secretion. We have studied the effect of constant light on lactate dehydrogenase (LDH; EC 1.1.1.27) and its isozyme C4 activities and protein content in whole epididymis, epididymal tissue and in spermatozoa from caput and cauda segments. Animals were exposed from birth to an illumination schedule of 14 h light:10 h dark (group L:D). At 60 days of age one group of animals was submitted to constant light over 50 days (group L:L). In order to test the fertilizing ability, the rats of each group were mated with soliciting estrous females. The percentage of pregnancies in females mated with males maintained in L:L was remarkably lower than those in females mated with males maintained in the L:D photoperiod (44% and 88% respectively). Constant light increased protein concentration and LDH activity in caput as well as in cauda of total epididymis. On the contrary, in epididymal tissue, the protein content decreased in both epididymal sections compared with controls. When enzymatic activity was expressed in Units per spermatozoa, constant light induced a significant reduction of total LDH and LDHC4 in caput and cauda spermatozoa while LDH activity of epididymal tissue was not affected. In spite of the decrease in LDH per sperm cell when rats were exposed to constant light, in total epididymis (epididymis tissue plus sperm cells content) and in spermatozoa, values of enzyme activities expressed per weight unit were higher than those of controls. This is explained by the increase in the amount of stored spermatozoa, both in caput and cauda, produced by exposure of animals to constant light. Our results confirm that in rats, chronic exposure to constant light promotes a reduction of fertilizing ability and indicates that continuous lighting reduces the total LDH and LDHC4 activities, possibly due to moderate aging of spermatozoa within the duct by lengthening of the sperm transit through the epididymis.     

Long-term administration of aqueous garlic extract (AGE) alleviates liver fibrosis and oxidative damage induced by biliary obstruction in rats

The aim of this study was to assess the antioxidant and antifibrotic effects of chronic administration of aqueous garlic extract on liver fibrosis induced by biliary obstruction in rats. Liver fibrosis was induced in male Wistar albino rats by bile duct ligation and scission (BDL). Aqueous garlic extract (AGE, 1 ml/kg, i.p., corresponding to 250 mg/kg) or saline was administered for 28 days. At the end of the experiment, rats were killed by decapitation. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) levels were determined to assess liver functions and tissue damage, respectively. Tumor necrosis factor-alpha (TNF-alpha) was also assayed in serum samples. Liver tissues were taken for determination of the free radicals, renal malondialdehyde (MDA) levels, an end product of lipid peroxidation; glutathione (GSH) levels, a key antioxidant; and myeloperoxidase (MPO) activity, as an indirect index of neutrophil infiltration. Hepatic collagen content, as a fibrosis marker was also determined. Serum AST, ALT, LDH, and TNF- alpha levels were elevated in the BDL group as compared to control group, while this increase was significantly decreased by AGE treatment. Hepatic GSH levels, significantly depressed by BDL, were elevated back to control levels in AGE-treated BDL group. Increases in tissue free radical and MDA levels and MPO activity due to BDL were reduced back to control levels by AGE treatment. Similarly, increased hepatic collagen content in the BDL rats was reduced to the level of the control group with AGE treatment. Since AGE administration alleviated the BDL-induced oxidative injury of the liver and improved the hepatic structure and function, it seems likely that AGE with its antioxidant and antifibrotic properties, may be of potential therapeutic value in protecting the liver fibrosis and oxidative injury due to biliary obstruction.     

Lactate dehydrogenase isoenzymes in the eye, cardiac and skeletal muscles of several decapods]

Properties of lactate dehydrogenase (LDH) in the eye, heart and muscles of Hemigrapsus sanguineus, Paralithodes camtschatica, Erimacrus isenbeckii, Pandalus latirastrus, Pagurus brachiomastus have been studied with acrylamide gel electrophoresis and kinetics analysis. LDH in all the tissues of all the representatives studied was found to be specific for L-pyruvate and lactate; it migrated in electrophoresis as a single band revealing low mobility towards anode. The isoenzyme from P. camtschatica and P. latirastrus differed from the isoenzymes of other animals studied by higher mobility towards anode that reflected higher negative value of its total charge. The LDH isoenzymes in all the animals studied resembled the A4 (LDH5) of the vertebrates being unstable to the denaturing action of high temperature and being unaffected by high concentrations of pyruvate up to 1.0.10-3M. On the other hand, in conrast to the A4 of mammals, the LDH in question displayed enhancement of the reaction rate and decrease of the Km values upon increase in the NAD+ and NAD.H concentrations both in the presence of high or low lactate and pyruvate concentrations. The isoenzymes displayed catalytic activity also in the presence of NADP, the Km values for pyruvate in the presence of equimolar (2.25 mM) concentrations of NAD.H or NADP.H were practically identical and were found to be within the limits of 14-26.10-5 M. Molecular weight of the LDH studied assessed by the gel filtration method was found to be 130-140,000. It is suggested that the LDH isoenzyme from the representatives of the decapod crayfish studied is homologous in its certain properties to the homotetrameric A4 form of the vertebrates.     

Changes in the activities of enzymes, especially lactate dehydrogenase, in endotoxin-poisoned mice.

Carbohydrate metabolic disorders were investigated by means of enzyme activities in mice (ddYS) injected intraperitoneally with endotoxin from Salmonella typhimurium. The mice exhibited hyperglycemia 2 hr after administration of endotoxin and hypoglycemia at 18 hr. Activity of hepatic phosphorylase in the endotoxin-poisoned mice at 2 hr was slightly higher than that in the control mice, whereas the level of this activity was not significantly different from that in the controls after 18 hr. Glucose-6-phosphatase activity in the poisoned mice increased by 2 hr after injection, but decreased by 18 hr. The blood lactate level in the poisoned mice transiently decreased until 3 hr after injection, but the mice exhibited a marked lactacidemia by 8–24 hr. The time course of lactate dehydrogenase (LDH) activity in various tissues was examined in mice injected with endotoxin. The activity of hepatic LDH declined to about two-thirds of that of the control mice after 16 hr, and was restored to the normal level by 48 hr. LDH in the cardiac muscle was markedly activated (by about 37%) in the early period (3–6 hr) after administration of endotoxin, and this activity gradually declined. However, the activity of LDH in the skeletal muscle showed a tendency similar to the rise and fall of the levels of blood lactate, and was restored to the normal value at 72 hr after injection. On the other hand, the serum LDH activity in the poisoned mice increased about 1.75-fold by 16 hr after injection. Mice injected with endotoxin exhibited a leakage of the isozymes LDH 3 and 5, but the origin of the leakage is uncertain. Similar elevation in the activities of transaminases (GPT and GOT) and malate dehydrogenase was found in the mouse serum at 16 hr after injection of endotoxin.