Liver Lactate Dehydrogenase Activity Research Articles

Ameliorative effect of piracetam on emamectin benzoate induced perturbations in the activity of lactate dehydrogenase in murine system

Emamectin benzoate (4´-deoxy-4´-epimethylaminoavermectin B1) is a macrocyclic lactone developed for the control of insect pests in edible plant crops. The current study was taken to assess the possible ameliorative effect of piracetam (P) on emamectin benzoate (EMB) induced alterations in energy metabolism in liver, kidney, testis, heart, cerebral cortex, cerebellum and muscle of rats. Rats of normal control group (N) received water and normal diet ad libitum and (EMB as well as EMB+P) group received 5 mg/kg bw emamectin benzoate via drinking water for 4 weeks. After four weeks of EMB treatment, rats of (EMB+P) received piracetam (500 mg/kg bw, iv) for 15 days. The results demonstrate that emamectin benzoate caused a significant increase in lactate dehydrogenase activity and the level of lactate indicating organ damage in treated animals. Piracetam, the so-called ‘nootropic’ drug is mainly used to treat cognitive impairment in aging, brain injuries, as well as dementia. In the present study piracetam treatment caused a significant inhibition of lactate dehydrogenase activity in liver, kidney, testis, heart, cerebral cortex, cerebellum and muscle of rats. The amelioration of toxic effects by piracetam treatment in EMB treated rats indicate that this drug has the potential to mitigate emamectin benzoate induced toxicity in mammalian systems.

In Vivo Magnetic Resonance Spectroscopy of Hyperpolarized [1-13 C]Pyruvate and Proton Density Fat Fraction in a Guinea Pig Model of Non-Alcoholic Fatty Liver Disease Development After Life-Long Western Diet Consumption.

Alterations in glycolysis are central to the increasing incidence of non-alcoholic fatty liver disease (NAFLD), highlighting a need for in vivo, non-invasive technologies to understand the development of hepatic metabolic aberrations. To use hyperpolarized magnetic resonance spectroscopy (MRS) and proton density fat fraction (PDFF) magnetic resonance imaging (MRI) techniques to investigate the effects of a chronic, life-long exposure to the Western diet (WD) in an animal model resulting in NAFLD; to investigate the hypothesis that exposure to the WD will result in NAFLD in association with altered pyruvate metabolism. Prospective. Twenty-eight male guinea pigs weaned onto a control diet (N=14) or WD (N=14). 3 T; T1-weighted gradient echo, T2-weighted spin-echo, three-dimensional gradient multi-echo fat-water separation (IDEAL-IQ), and broadband point-resolved spectroscopy (PRESS) chemical-shift sequences. Median PDFF was calculated in the liver and hind limbs. [1-13 C]pyruvate dynamic MRS in the liver was quantified by the time-to-peak (TTP) for each metabolite. Animals were euthanized and tissue was analyzed for lipid and cholesterol concentration and enzyme level and activity. Unpaired Student's t-tests were used to determine differences in measurements between the two diet groups. The Pearson correlation coefficient was calculated to determine correlations between measurements. Life-long WD consumption resulted in significantly higher liver PDFF and elevated triglyceride content in the liver. The WD group exhibited a decreased TTP for lactate production, and ex vivo analysis highlighted increased liver lactate dehydrogenase (LDH) activity. PDFF MRI results suggest differential fat deposition patterns occurring in animals fed a life-long WD characteristic of lean, or lacking excessive subcutaneous fat, NAFLD. The decreased liver lactate TTP and increased ex vivo LDH activity suggest lipid accumulation occurs in association with a shift from oxidative metabolism to anaerobic glycolytic metabolism in WD-exposed livers. 2 TECHNICAL EFFICACY STAGE: 1.

Punicalagin Reversed the Hepatic Injury of Tetrachloromethane by Antioxidation and Enhancement of Autophagy.

Hepatic injury is significant in the pathogenesis and development of many types of liver diseases. Punicalagin (PU) is a bioactive antioxidant polyphenol found in pomegranates. To explore its protective effect against carbon tetrachloride (CCl4)-induced liver injury and the mechanism, Institute of Cancer Research (ICR) mice and L02 cells were used to observe the changes of serum biochemical indicators, histopathological liver structure, cell viability, antioxidative indices, and autophagy-related proteins were assessed. In ICR mice, PU ameliorated the CCl4-induced increase of the serum aspartate aminotransferase, alanine aminotransferase, the activity of liver lactate dehydrogenase, and the damage of histopathological structure, and exhibited a hepatoprotective effect against CCl4. PU attenuated oxidative stress by decreasing the liver malondialdehyde level and increasing the activities of liver superoxide dismutase, glutathione peroxidase, and the expression of the liver nuclear factor E2-related factor (Nrf2) protein. Furthermore, according to the vivo and vitro experiments, PU might activate autophagy through the mediation of the Akt/FOXO3a and P62/Nrf2 signaling pathway. Taken together, these results suggest that PU may protect against CCl4-induced liver injury through the upregulation of antioxidative activities and autophagy.

Re: Reduction in Urinary Oxalate Excretion in Mouse Models of Primary Hyperoxaluria by RNA Interference Inhibition of Liver Lactate Dehydrogenase Activity.

Re: Reduction in Urinary Oxalate Excretion in Mouse Models of Primary Hyperoxaluria by RNA Interference Inhibition of Liver Lactate Dehydrogenase Activity.

Reduction in urinary oxalate excretion in mouse models of Primary Hyperoxaluria by RNA interference inhibition of liver lactate dehydrogenase activity

The Primary Hyperoxaluria's (PH) are rare autosomal recessive disorders characterized by elevated oxalate production. PH patients suffer recurrent calcium oxalate kidney stone disease, and in severe cases end stage renal disease. Recent evidence has shown that RNA interference may be a suitable approach to reduce oxalate production in PH patients by knocking down key enzymes involved in hepatic oxalate synthesis. In the current study, wild type mice and mouse models of PH1 (AGT KO) and PH2 (GR KO) were treated with siRNA that targets hepatic LDHA. Although siRNA treatment substantially reduced urinary oxalate excretion [75%] in AGT KO animals, there was a relatively modest reduction [32%] in GR KO animals. Plasma and liver pyruvate levels significantly increased with siRNA treatment and liver organic acid analysis indicated significant changes in a number of glycolytic and TCA cycle metabolites, consistent with the known role of LDHA in metabolism. However, siRNA dosing data suggest that it may be possible to identify a dose that limits changes in liver organic acid levels, while maintaining a desired effect of reducing glyoxylate to oxalate synthesis. These results suggest that RNAi mediated reduction of hepatic LDHA may be an effective strategy to reduce oxalate synthesis in PH, and further analysis of its metabolic effects should be explored. Additional studies should also clarify in GR KO animals whether there are alternate enzymatic pathways in the liver to create oxalate and whether tissues other than liver contribute significantly to oxalate production.

Biochemical response to acute temperature change in Atlantic killifish, Fundulus heteroclitus (586.1)

It is documented that after temperature acclimation, the killifish Fundulus heteroclitus shows differences in the activities of a number of enzymes including lactate dehydrogenase (LDH), an important catalyst in anaerobic respiration. Less well understood is the temporal pattern of change in activity from one temperature to another. We acclimated fish to 22°C, and shifted the temperature such that an equilibrium was reached at 4°C after 9 hours. During the shift, we collected liver and white muscle samples and assayed homogenates for the specific activity of LDH. After three hours, LDH activity in liver increased from 22.2 µmol·min‐1·mg protein‐1 to 75.1 µmol·min‐1·mg protein‐1 , but then dropped by nine hours to 25.4 µmol·min‐1·mg protein‐1. Conversely, LDH activity in muscle decreased from 154 µmol·min‐1·mg protein‐1 to 61.3 µmol·min‐1·mg protein‐1 and continued to decrease at a slowed rate. These data demonstrate that F. heteroclitus adjusts LDH activity extremely rapidly in response to temperature change. We are currently determining the response to the opposite temperature shift (4 to 22°C), and we plan to assess several enzymes associated with aerobic respiration and other aspects of metabolism. Together, these analyses will help us determine which major metabolic pathways are most critical to this species during rapid temperature change.Grant Funding Source: Supported by the Guerrieri Foundation and the Salisbury University Department of Biological Sciences

Effect of Simulated Microgravity on the Activity of Regulatory Enzymes of Glycolysis and Gluconeogenesis in Mice Liver

Gravity supports all the life activities present on earth. Microgravity environments have effect on the biological functions and physiological status of an individual. The present study was undertaken to investigate the effect of simulated microgravity on important regulatory enzymes of carbohydrate metabolism in liver using HLS mice model. Following hind limb unloading of mice for 11 days the animal’s average body weights were found to be not different, while the liver weights were decreased and found to be significantly different (p < 0.05) from control mice. Further, in liver the specific activity of hexokinase enzyme was reduced (p < 0.02) and the phosphoenolpyruvate carboxykinase activity was significantly increased in simulated microgravity subjected mice compared to control (p < 0.003). Immunoblot analysis show decreased phosphofructokinase-2 activity in HLS mice compared to control. Liver lactate dehydrogenase activity significantly reduced in simulated microgravity subjected mice (p < 0.005). Thus in our study the rodents have adapted to simulated microgravity conditions, with decreased glycolysis and increased gluconeogenesis in liver and reciprocally regulated.

Vinpocetine protects liver against ischemia–reperfusion injury

Hepatic ischemia-reperfusion (IR) injury is a clinical problem that leads to cellular damage and organ dysfunction mediated mainly via production of reactive oxygen species and inflammatory cytokines. Vinpocetine has long been used in cerebrovascular disorders. This study aimed to explore the protective effect of vinpocetine in IR injury to the liver. Ischemia was induced in rats by clamping the common hepatic artery and portal vein for 30 min followed by 30 min of reperfusion. Serum transaminases and liver lactate dehydrogenase (LDH) activities, liver inflammatory cytokines, oxidative stress biomarkers, and liver histopathology were assessed. IR resulted in marked histopathology changes in liver tissues coupled with elevations in serum transaminases and liver LDH activities. IR also increased the production of liver lipid peroxides, nitric oxide, and inflammatory cytokines interleukin-1β and interleukin-6, in parallel with a reduction in reduced glutathione and interleukin-10 in the liver. Pretreatment with vinpocetine protected against liver IR-induced injury, in a dose-dependent manner, as evidenced by the attenuation of oxidative stress as well as inflammatory and liver injury biomarkers. The effects of vinpocetine were comparable with that of curcumin, a natural antioxidant, and could be attributed to its antioxidant and anti-inflammatory properties.

Biochemical and histopathological changes induced by different time intervals of methomyl treatment in mice liver

The present study was designed to evaluate the toxic effects induced by different time intervals of methomyl exposure on liver antioxidant defense system, oxidative stress, liver function biomarkers and histopathology in CD-1 mice. Ten male mice per group were assigned to one of four treatment groups. Group one served as control while group 2, 3 and 4 were orally treated with one mg methomyl/kg BW for 10, 20 and 30 days, respectively. Results obtained showed that methomyl significantly induced TBARS and decreased the activity of antioxidant enzymes, glutathione S-transferase, superoxide dismutase and catalase and the levels of reduced glutathione in mice liver. Aminotransferases and alkaline phosphatase activities were significantly decreased in liver due to methomyl administration, while the activities of these enzymes were significantly increased in serum. In addition, liver lactate dehydrogenase activity was significantly increased. On the contrary, methomyl treatment caused a significant decrease in liver acid phosphatase. The histology of mice liver treated with methomyl for 10, 20 and 30 days of duration showed dilation of central vein, sinusoids between hypertrophied hepatocytes and nuclear degeneration with mononuclear cell infiltration. In conclusion, exposure to methomyl induced toxicity and oxidative stress in mice liver via free radicals mechanism. Also, methomyl might have affected cell metabolism, cell membrane permeability and the detoxification system in liver.

The effect of hypoxia on intermediary metabolism and oxidative status in gilthead sea bream (Sparus aurata) fed on diets supplemented with methionine and white tea

The present study evaluates the influence of previous nutritional status, fish fed on diets supplemented with tea and methionine, on acute hypoxia tolerance and subsequent recovery of Sparus aurata juveniles. Four isonitrogenous (45% of protein) and isolipidic (18% lipid) diets were formulated to contain 0.3% methionine, 2.9% white tea dry leaves or 2.9% of white tea dry leaves+0.3% methionine. An unsupplemented diet was used as control. Hepatic key enzymes of intermediary metabolism and antioxidant status, superoxide dismutase isoenzyme profile, glutathione (total, reduced and oxidized) and oxidative damage markers were determined under normoxia, hypoxia challenge and during normoxia recovery. Dietary white tea inclusion decreased plasma glucose levels under normoxia and seemed to induce an increase in anaerobic pathways as showed by enhanced liver lactate dehydrogenase activity. Hypoxia challenge reversed some of the responses induced by diet tea supplementation. Hypoxia decreased plasma glucose levels, increased glucose 6-P-dehydrogeanse activity, decreased superoxide dismutase activity (especially Mn-SOD and CuZn-SOD isoforms) and increased glutathione peroxidase activity in all dietary treatments. Catalase activity during hypoxia varied with dietary treatments and glutathione reductase was not modified. Antioxidant defenses were insufficient to avoid an oxidative stress condition under hypoxia, independently of dietary treatment. In general, pre-challenge values were recovered for almost all parameters within 6h recovery time.

Effect of dietary Mintrex-Zn/Mn on performance, gene expression of Zn transfer proteins, activities of Zn/Mn related enzymes and fecal mineral excretion in broiler chickens

This study was to evaluate dietary Mintrex-Zn/Mn on growth performance, enzyme activities, and trace mineral absorption and utilization in 0–3-wk broilers. One hundred sixty day-old male broiler chickens were allotted to 4 dietary treatments with 5 replicate cages of 8 birds. Broilers were fed maize-soybean basal diets containing zinc (Zn, 100 mg/kg) and manganese (Mn, 120 mg/kg) from sulphate salts, while three other treatments included 100%, 80%, and 60% of the basal dietary mineral (actually 70%, 56% and 42% of sulphate salts based on 70% of sulphates would be available) from Mintrex-Zn/Mn, respectively. At the end of 3 weeks of age, the growth performance, mRNA abundance of Zn/Mn transfer proteins in jejunum mucosa, enzyme activities of liver lactate dehydrogenase (LDH), glutamic oxalacetic transaminase (GOT) and glutamate-pyruvate transaminase (GPT), activities of serum alkaline phosphatase (ALP), Mn-superoxide dismutase (SOD), total superoxide dismutase (T-SOD) and CuZn-SOD and bone mineralization were measured. Total collection procedure in the balance trial of excreta was done from the age of 20 to 23 days. The results showed that supplementation with 100% Mintrex-Zn/Mn significantly improved the average daily gain (ADG) (P<0.01) and decreased fecal mineral excretion (P<0.05) compared to inorganic supplementation, but did not affect Zn/Mn transfer proteins mRNA abundance ( P > 0.05). Supplementation with 80% Mintrex-Zn/Mn lowered serum ALP activity (P<0.05), however, it did not affect the growth performance, mRNA abundance of Zn/Mn transfer proteins and bone mineralization in comparison to inorganic supplementation ( P > 0.05). The decrease of excretion is mainly due to the reduction of dietary supplemental level of minerals. Supplementation with 80% Mintrex-Zn/Mn decreased Mn and Zn excretion in the feces (mg/kg diet) by 39.79% and 30.13% (P<0.001), respectively. Supplementation with 60% Mintrex-Zn/Mn significantly decreased ADG (P<0.01), the length of metatarsus, serum ALP activities and mRNA expression of Zn transfer proteins but increased mortality and culling rate (P<0.05). There were no differences in activities of serum T-SOD, CuZn-SoD and Mn-SOD, and liver metabolic enzyme (LDH, GOT, and GPT) among inorganic versus Mintrex Zn/Mn supplementations. This study suggested that using approximately 30–40% Mintrex Zn/Mn could not substitute for the inorganic trace mineral. LDH, GOT, GPT may not be sensitive variables to reflect the states of the Zn and Mn in the body. Supplementation with 80% Mintrex-Zn/Mn (56% of inorganic mineral level) had a better effect in reducing the fecal mineral excretion without compromise in the growth performance. Using relative mineral concentration in fecal material may overestimate the values of mineral reduction, and it would be more accurate to use trace mineral concentration per chick day or per kg diet intake.

Protective Effect of Mentha piperita against Arsenic‐Induced Toxicity in Liver of Swiss Albino Mice

The protective role of leaves of Mentha piperita Linn (Mint) was studied in adult Swiss albino mice against arsenic-induced hepatopathy. The animals were divided into four groups. Group I: only vehicle (0.9% NaCl) was administered. Group II: the animals received Mentha leaf extract (1 g/kg body weight per day) orally for 30 days. Group III: animals were treated with sodium arsenite (4 mg/kg body weight) intraperitoneally in 0.9% NaCl. Group IV: animals were given Mentha extract for 10 consecutive days prior to sodium arsenite treatment and continuously for 30 days after sodium arsenite treatment. The animals from the above groups were killed at various time-points, and body weight and liver weight were measured. The biochemical estimation of lipid peroxidation (LPO), reduced glutathione (GSH), lactate dehydrogenase (LDH), acid phosphatase (ACP), and alkaline phosphatase (ALP) in liver and serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT) in serum were done. In the arsenic-treated group there was a significant increase in ACP, ALP, SGOT, SGPT and LPO content, whereas a significant decrease was recorded in body weight, liver weight, GSH and LDH activity in liver. Pre- and post-treatment of Mentha with arsenic significantly alters the biochemical parameters in liver. A significant decline in ACP, ALP, SGOT, SGPT and LPO content was observed. However, a significant increase in body weight, liver weight, GSH content and LDH activity in liver was estimated. The results indicate that the Mentha extract may be useful in reducing the side effects of arsenic-induced hepatopathy.

Hypoglycemic activity of Jatrorrhizine

The hypoglycemic activity and its mechanism of Jatrorrhizine (Jat) were studied. The normal mice and alloxan-induced hyperglycemic mice were given with different doses of Jat. Blood glucose and liver glycogen levels were determined by spectrophotometry with glucose-oxidase and iodine reagents respectively. The levels of blood lactic acid (LC) and liver lactate dehydrogenase (LDH) activity were measured to explore the effect of Jat on anaerobic glycolysis. Succinate dehydrogenase (SDH) activity in liver was measured to evaluate the effect of Jat on aerobic glycolysis in liver. It was found that Jat (50 mg/kg, 100 mg/kg) could significantly decrease blood glucose level in a dose- and time-dependent manner in both normal and alloxan-diabetic mice, increase the activity of SDH, but had no significant effects on the LC level and LDH activity. Jat could significantly reduce the content of liver glycogen in normal mice. Moreover, Jat could inhibit the platelet aggregation in rabbits in vitro in a dose-effect relationship. It was concluded that Jat induced the pronounced decrease in blood glucose in normal and hyperglycemic mice. The hypoglycemic activity of Jat may be attributed to the enhancement of aerobic glycolysis.

Counteraction of oxalate induced nitrosative stress by supplementation of l-arginine, a potent antilithic agent

Background Our understanding of nitrosative stress in the process of urolithiasis is far from complete. Earlier studies carried out in our laboratory demonstrate the presence of nitrated THP in stone formers, l-arginine ( l-arg) a precursor of nitric oxide (NO), attenuates the endothelial dysfunction caused by reactive nitrogen species. We investigated the role of l-arg in ethylene glycol (EG)-induced urolithic rat model and observed its antilithic and antioxidative properties. Methods Hyperoxaluria was induced using 0.75% EG in drinking water. l-arg [1.25 g/kg body weight] was given orally for a period of 28 days. Results EG-treated rats showed significant loss in body weight and increase in the activities of oxalate synthesizing enzymes such as glycollic acid oxidase in liver. Lactate dehydrogenase activity in liver and kidney was increased. The activity of the free radical producing enzyme xanthine oxidase, tissue oxalate and calcium levels were significantly increased in EG-treated rats. Depletion in the antioxidant enzymes, membrane bound ATPases and thiol status was observed in these rats. l-arg co-supplementation to EG-treated rats maintained the activities of the oxalate synthesizing enzymes and free radical producing enzymes with in the normal range. Tissue oxalate and calcium levels were also maintained near normal in l-arg treated hyperoxaluric rats. l-arg, by its cytoprotective effect, maintained the thiol status, thereby preserving the activities of the membrane bound ATPases and preventing proteinuria and subsequent weight loss in EG-treated rats. Conclusion l-arg feeding prevents the retention of calcium oxalate crystals in hyperoxaluric rats by way of protecting the renal cells from oxidative injury and also by providing a second line of defense through the normalization of the oxalate metabolism. It reduces the risk of stone formation, by curtailing free radicals and hyperoxaluria as both of them have to work in close association to form stones.

Prospective protective role of melatonin against arsenic-induced metabolic toxicity in Wistar rats

Subchronic exposure to arsenic is associated with alteration of glucose homeostasis. Arsenic treatment (as sodium arsenite) of male Wistar rats (weighing 130-150 g) at a dose of 5.55 mg kg(-1) body weight (equivalent to 35% of LD(50)) (i.p.) per day for a period of 30 days produced hypoglycemia, with associated increased urinary excretion of glucose and depletion of liver glycogen and pyruvic acid contents. Mobilization of free amino acids from kidney to liver was facilitated by arsenic treatment. Arsenic exposure significantly decreased the glutamate-pyruvate transaminase activity in kidney. Glucose 6-phosphatase activity in liver tissue was also significantly decreased after arsenic treatment. In addition to these, liver lactate dehydrogenase activity was elevated due to arsenic treatment. Melatonin supplementation (i.p.) at a dose of 10 mg kg(-1) day(-1) for last five days prior to sacrifice reversed most of the above changes caused by arsenic. Melatonin, being a potent free radical scavenger may reduce arsenic-induced free radical production, and thereby, eliminating its toxic effects. So, arsenic-induced hypoglycemia, with associated glycogenolytic as well as glycolytic activities of liver can be partially counteracted by melatonin supplementation. Accordingly, it may be suggested that melatonin can serve as a prospective protective agent against arsenic-induced metabolic toxicity.

Interdemic variation in haematocrit and lactate dehydrogenase in the African cyprinid Barbus neumayeri

This study evaluated whether the African cyprinid Barbus neumayeri from Rwembaita Swamp (low‐oxygen) and Njuguta River (high‐oxygen) in the Kibale National Park, Uganda differed in traits related to aerobic and anaerobic metabolic potential. Haematocrit was measured as an index of blood oxygen‐carrying capacity, and tissue activities and isozyme composition of lactate dehydrogenase (LDH) were measured as indices of tissue anaerobic capacity. To address whether site‐dependent differences were acute responses v. longer‐term adjustments to environmental conditions, these variables were measured in fish sampled shortly after collection and after laboratory maintenance under well‐aerated conditions. In fish sampled in the field, those from the low‐oxygen site had significantly higher haematocrit, but this difference disappeared after long‐term laboratory maintenance. In contrast, fish from the low‐oxygen site had higher liver LDH activities than fish from the high‐oxygen site, and this difference persisted during laboratory maintenance. Polymorphism was detected at both the LDH‐A and LDH‐B loci, and genotype frequencies for LDH‐B differed significantly between collection sites. These results demonstrate physiological, biochemical and genetic differences in B. neumayeri from habitats differing in dissolved oxygen availability and suggest both acute and long‐term responses to local environmental conditions.

The Influence of Dietary Grapeseed Oil on DMBA-Induced Liver Enzymes Disturbance in the Frog, Rana ridibunda

The current study was designed to determine whether dietary grapeseed oil inhibits liver cytotoxicity induced by 7,12- dimethylbenz(a)anthracene (DMBA) in the frog, Rana ridibunda. The experimental animals were divided into five groups and treated for 2 weeks with 7,12- dimethylbenz(a)anthracene, DMBA plus grapeseed oil, grapeseed oil, olive oil and last group was untreated and used as control. Liver enzymes, lactate dehydrogenase, glutamic oxaloacetic acid transaminase, glutamic pyruvic acid transaminase and alkaline phosphatase were chosen to assess liver function. In comparison with control, the administration of DMBA alone significantly elevated the activity of liver lactate dehydrogenase, while the activities of glutamic oxaloacetic acid transaminase, glutamic pyruvic acid transaminase and alkaline phosphatase were declined. Similar results were noted in frogs treated with DMBA plus grapeseed oil. Moreover, it is found that the changes were more pronounced in frogs treated with DMBA plus grapeseed oil than those treated with DMBA. The activities of these enzymes in frogs exposed to grapeseed oil or olive oil were not significantly different from those of controls. These results indicate that grapeseed oil effectively increases DMBA-induced hepatotoxicity in the frogs. Also, the results suggested that grapeseed oil has enhancing effects of DMBA metabolic activation.

Radiomodifying Potential of Panax ginseng in Liver of Swiss Albino Mice against Gamma Radiation

Panax ginseng occupies an important role in the folk medicine of China, Korea and Japan. The present study was undertaken to determine the radioprotective efficacy of ginseng root extract in the liver of Swiss albino mice. The animals were divided into 4 groups. Group I-Only vehicle was administered. Group II-The animals received 10 mg/kg body weight ginseng root extract i.p. for 4 consecutive days. Group III-Animals were irradiated with 8Gy gamma radiation at the dose rate of 1.69 Gy/min at the distance of 80 ems. Group IV-Animals were given by ginseng root extract (10 mg/kg body weight) continuously for 4 days and on 4th day they were irradiated with 8 Gy gamma radiation after 30 min. The animals from above groups were autopsied on 1,3,7,14 and 30 days. Biochemical estimations of phosphatases (acid ＆ alkaline), LDH (lactate dehydrogenase), LPO (lipid peroxidation) and GSH (reduced glutathione) in liver and SGOT (serum glutamate oxaloacetate transaminase), SGPT (serum glutamate pyruvate transaminase) and alkaline phosphatase in serum were done. In ginseng treated group acid phosphatase (ACP), alkaline phosphatase (ALP), LPO and LDH in liver and SGOT, SGPT and alkaline phosphatase in serum did not show any significant alteration. However, a significant increase in GSH content in liver was recorded. In irradiated group there was a significant increase in ACP, ALP and LPO content in liver and SGOT ＆ SGPT in serum was noted. Whereas, a significant decrease was recorded in GSH and LDH activity in liver and alkaline phosphatase activity in serum. Pretreatment of ginseng with radiation significantly alters the biochemical parameters in liver and serum. A significant decline in ACP, ALP activity and LPO content in liver and SGOT and SGPT activity in serum was observed. However, a significant increase in GSH content and LDH activity in liver and ALP activity in serum was estimated. The present study suggests that pretreatment of ginseng before irradiation significantly protects the liver and maintains the enzyme activity.

Protective Effect of N‐Acetylcysteine Against Arsenic‐Induced Depletion In Vivo of Carbohydrate

N‐acetylcysteine (NAC), a synthetic aminothiol, possesses antioxidative and cytoprotective properties. The present study evaluates the effect of NAC supplementation on arsenic‐induced depletion in vivo of carbohydrates. Arsenic (as sodium arsenite) treatment (i.p.) of male Wistar rats (120–140 g b.w.) at a dose of 5.55 mg/kg body weight (35% of LD50) per day for a period of 30 days produced a significant decrease in blood glucose level (hypoglycemia) and a fall in liver glycogen and pyruvic acid contents. The free amino acid nitrogen content of liver increased while that of kidney decreased after arsenic treatment. Arsenic also enhanced the liver lactate dehydrogenase activity whereas glucose 6‐phosphatase activity in both liver and kidney decreased significantly following arsenic treatment. Transaminase activities in liver and kidney were not significantly altered except the glutamate–pyruvate transaminase activity that was reduced in kidney after arsenic treatment. Oral administration of NAC (163.2 mg/kg/day) for last 7 days of treatment prevented the arsenic‐induced hypoglycemia and glycogenolytic effects to an appreciable extent. There was also recovery of liver pyruvic acid as well as liver and kidney free amino acid nitrogen content after NAC supplementation. Arsenic‐induced alteration of glucose 6‐phosphatase activity in both liver and kidney was also counteracted by NAC. It is suggested that carbohydrate depletion in vivo due to exposure to arsenic can be counteracted by NAC supplementation.

Metabolic adjustments in the common carp during prolonged hypoxia

Biochemical and respiratory changes in the common carp Cyprinus carpio, were studied 6, 24, 96 and 168 h upon exposure to hypoxia (0·5 mgO2 l−1). Modification of kinetic properties of phosphofructokinase (PFK‐1), coupled with a decreased in PFK‐1 activities, were evident in muscle. No changes in kinetics and activities could be observed in muscle pyruvate kinase (PK) and lactate dehydrogenase (LDH). A decrease in muscle citrate synthase (CS) and an increase in muscle cytochrome c oxidase (CCO) were found. The common carp was able to maintain a constant level of muscle glycogen, muscle ATP, and liver CS throughout the 168‐h experimental period. Changes in activities of liver LDH and muscle CCO were observed only at 168 h, which indicates that common carp may switch to alternative metabolic pathway to deal with prolonged hypoxia. A severe decrease in liver glycogen was accompanied by increases in lactate levels in both the muscle and liver. Oxygen consumption rate was reduced under hypoxia, but resumed to normoxic levels within 2 h upon return to normoxic condition. Overall, these results indicate that carp adopt different strategies in an attempt to deal with short term and long term hypoxia in the natural environment.