Lactate Dehydrogenase In Tissues Research Articles

Distribution of isozyme spectra of lactate dehydrogenase in tissues of invasive species mammals of Karelia

Distribution of isozyme spectra of lactate dehydrogenase in tissues of invasive species mammals of Karelia

Protective role of selenium and selenium-nanoparticles against multiple stresses in Pangasianodon hypophthalmus.

Pollution and climate change pose significant threats to aquatic ecosystems, with adverse impacts on aquatic animals, including fish. Climate change increases the toxicity of metal in aquatic ecosystems. To understand the severity of metal pollution and climate change, an experiment was conducted to delineate the mitigation potential of selenium (Se) and selenium nanoparticles (Se-NPs) against lead (Pb) and high temperature stress in Pangasianodon hypophthalmus.For the experiment, five isonitrogenous and isocaloric diets were prepared, varying in selenium supplementation as Se at 0, 1, and 2 mg kg-1 diet, and Se-NPs at 1 and 2 mg kg-1 diet. The fish in stressor groups were exposed to Pb (1/20th of LC50 concentration, 4 ppm) and high temperature (34 °C) throughout the experiment. The results demonstrated that dietary supplementation of Se at 1 and 2 mg kg-1 diet, as well as Se-NPs at 1 mg kg-1 diet, significantly reduced (p< 0.01) the levels of lactate dehydrogenase and malate dehydrogenase in both liver and muscle tissues. Additionally, the levels of alanine aminotransferase and aspartate aminotransferase in both gill and liver tissues were significantly decreased (p< 0.01) with the inclusion of Se and Se-NPs in the diets. Furthermore, the enzymes glucose-6-phosphate dehydrogenase in gill and liver tissues, fructose 1,6-bisphosphatase in liver and muscle tissues, and acid phosphatase in liver tissue were remarkably reduced (p< 0.01) due to the supplementation of Se and Se-NPs. Moreover, dietary supplementation of Se and Se-NPs significantly enhanced (p< 0.01) the activity of pyruvate kinase, glucokinase, hexokinase, alkaline phosphatase, ATPase, protease, amylase, lipase, and RNA/DNA ratio in the fish. Histopathological examination of gill and liver tissues also indicated that Se and Se-NPs protected against structural damage caused by lead and high-temperature stress. Moreover, the study examined the bioaccumulation of selenium and lead in muscle, water, and diets. The aim of the study revealed that Se and Se-NPs effectively protected the fish from lead toxicity and high-temperature stress, while also improving the function of cellular metabolic enzymes in P. hypophthalmus.

Toxic Effect of Silver Nanoparticles on Liver, Gill and Muscle Tissues of Zebrafish &lt;i&gt;Danio rerio&lt;/i&gt;

The present study was aimed to evaluate the toxic effect of Silver nanoparticle on the liver, gill and muscle tissues of the Zebrafish, Danio rerio. The experiment was designed to understand the chronic toxicity of silver nanoparticles (AgNPs) in adult fish, Danio rerio. In the chronic toxicity study adult fish, Danio rerio were divided in to two groups. First group was experimental group in which fish were successively treated with a graded series of 0.3, 0.6, 0.9 mg/l an average 60 nm. PVP. coated AgNPs treatment were given for 21 days, at the end of experimental period, Reduced glutathione activity (GSH), Lipid peroxidation activity (LPO), Lactate dehydrogenase (LDH) and Total protein in liver, gill and muscle tissues were assayed. Second group were kept as a control which was free from AgNPs exposure. The levels of Reduced glutathione activity (GSH) and Total protein were found to be decreased were as Lipid peroxidation activity (LPO) and Lactate dehydrogenase activity (LDH) were found to be elevated in liver, gill and muscle tissue of AgNPs treated Zebrafish Danio rerio.

Activation of AMPK/p38/Nrf2 is involved in resveratrol alleviating myocardial ischemia-reperfusion injury in diabetic rats as an endogenous antioxidant stress feedback.

BackgroundMyocardial necrosis caused by myocardial ischemia-reperfusion (MI/R) in diabetic patients is prominently aggravated and can cause oxidative stress. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a redox-sensing transcription factor that protects against myocardial ischemia/reperfusion injury (MIRI). However, the mechanism of action of Nrf2 in resveratrol-pretreated cardiomyocytes is complex. We assumed that adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/p38 mitogen-activated protein kinases (p38)/Nrf2 might be involved in resveratrol alleviating MIRI in diabetic rats as an endogenous protective mechanism.MethodsA total of 50 type 2 diabetes mellitus (T2DM) rat models were randomly divided into 5 groups (n=10 in each group): sham group; MI/R group; AMPK inhibitor compound C + myocardial ischemia-reperfusion (C + MI/R) group; resveratrol + myocardial ischemia-reperfusion (RSV + MI/R) group; and resveratrol + AMPK inhibitor compound C + myocardium ischemia-reperfusion group (RSV + C + MI/R) group. Rats were fed a high fat diet, and the T2DM models were established by intraperitoneal injection of 1% streptozotocin (STZ). The MIRI models were established by ligating the left anterior descending coronary artery for 30 minutes followed by reperfusion for 120 minutes. The size of myocardial infarction was measured. Serum samples were collected to measure the concentrations of creatine kinase-MB (CK-MB). The levels of lactate dehydrogenase (LDH), glutathione (GSH), and superoxide dismutase (SOD) in myocardial tissues were determined. Immunofluorescence analysis of translocase of outer mitochondrial membrane 20 (TOMM20) was performed to observe the pathological changes in myocardial tissues. The protein expressions of AMPK, p-AMPK, p38, p-p38, Nrf2, and heme oxygenase 1 (HO-1) were determined by western blotting.ResultsCompared with the sham group, the expressions of AMPK, p38, Nrf2, and HO-1 in the myocardium were significantly increased in the MI/R group. Compared with the MI/R group, the RSV + MI/R group had a significantly lower oxidative stress level, milder myocardial injury, increased expressions of AMPK, Nrf2, and HO-1, and lower expression of p38. The protein expressions of Nrf2 and HO-1 were partially inhibited in the RSV + C + MI/R group.ConclusionsResveratrol can inhibit oxidative stress and alleviate MIRI by activating the AMPK/p38/Nrf2 signaling pathway. Meanwhile, AMPK/p38/Nrf2 is also an endogenous antioxidant stress pathway that protects against stress.

Expression pattern and clinical significance of microRNA-let-7a and IFN-gamma in placental tissue of patients with preeclampsia with severe features.

Preeclampsia with severe features (PECsf) isacommon disease in pregnant women. let-7a and IFN-gamma (interferon-gamma) are involved in diagnosis and prognosis of preeclampsia. This study explored effects of let-7a and IFN-gamma on PECsf patients. The placental tissue of 21PECsf, 19 preeclampsia without severe features (PEC), and 20 normal pregnant women were collected, and clinical data were recorded. let-7a and IFN-gamma expressions in placental tissue were detected. The correlation between let-7a/IFN-gamma expression and clinical indexes was analyzed. According to let-7a and IFN-gamma expressions, PECsf patients were assigned into Hlet-7a group (let-7a high expression group), Llet-7a group (let-7a low expression group), HIFN-gamma group (IFN-gamma high expression group) and LIFN-gamma group (IFN-gamma low expression group). The incidence of adverse prognosis was compared. let-7a and IFN-gamma were highly expressed in placental tissue of preeclampsia patients, with significant differences between PEC and PECsf. The high expressions of let-7a and IFN-gamma were positively correlated with mean arterial pressure, lactate dehydrogenase, and 24h urinary protein in placental tissues of PECsf patients. High let-7a and IFN-gamma expressions were correlated with adverse outcomes of PECsf. High let-7a and IFN-gamma expressions were correlated with clinical features, and could be used as biomarkers for treatment and poor prognosis of PECsf.

A Review on the Medicinal and Pharmacological Properties of Traditional Ethnomedicinal Plant Sonapatha, Oroxylum indicum

Oroxylum indicum, Sonapatha is traditionally used to treat asthma, biliousness, bronchitis, diarrhea, dysentery, fevers, vomiting, inflammation, leukoderma, skin diseases, rheumatoid arthritis, wound injury, and deworm intestine. This review has been written by collecting the relevant information from published material on various ethnomedicinal and pharmacological aspects of Sonapatha by making an internet, PubMed, SciFinder, Science direct, and Google Scholar search. Various experimental studies have shown that Sonapatha scavenges different free radicals and possesses alkaloids, flavonoids, cardio glycosides, tannins, sterols, phenols, saponins, and other phytochemicals. Numerous active principles including oroxylin A, chrysin, scutellarin, baicalein, and many more have been isolated from the different parts of Sonapatha. Sonapatha acts against microbial infection, cancer, hepatic, gastrointestinal, cardiac, and diabetic disorders. It is useful in the treatment of obesity and wound healing in in vitro and in vivo preclinical models. Sonapatha elevates glutathione, glutathione-s-transferase, glutathione peroxidase, catalase, and superoxide dismutase levels and reduces aspartate transaminase alanine aminotransaminase, alkaline phosphatase, lactate dehydrogenase, and lipid peroxidation levels in various tissues. Sonapatha activates the expression of p53, pRb, Fas, FasL, IL-12, and caspases and inhibited nuclear factor kappa (NF-κB), cyclooxygenase (COX-2), tumor necrosis factor (TNFα), interleukin (IL6), P38 activated mitogen-activated protein kinases (MAPK), fatty acid synthetase (FAS), sterol regulatory element-binding proteins 1c (SREBP-1c), proliferator-activated receptor γ2 (PPARγ2), glucose transporter (GLUT4), leptin, and HPV18 oncoproteins E6 and E7 at the molecular level, which may be responsible for its medicinal properties. The phytoconstituents of Sonapatha including oroxylin A, chrysin, and baicalein inhibit the replication of SARS-CoV-2 (COVID-19) in in vitro and in vivo experimental models, indicating its potential to contain COVID-19 infection in humans. The experimental studies in various preclinical models validate the use of Sonapatha in ethnomedicine and Ayurveda.

Fucoxanthin alters the apelin-13/APJ pathway in certain organs of γ-irradiated mice.

Apelin-13 and APJ are implicated in different key physiological processes. This work aims at exploring the radioprotective effect of fucoxanthin (FX) on γ-radiation (RAD)-induced changes in the apelin-13/APJ pathway, which causes damage in the liver, kidney, lung and spleen of mice. Mice were administered FX (10 mg kg–1 day–1, i.p) and exposed to γ-radiation (2.5 Gy week–1) for four consecutive weeks. The treatment of irradiated mice by FX resulted in a significant amendment in protein expression of the apelin-13/APJ/NF-κB signalling pathway concurrently with reduced hypoxia (hypoxia-inducible factor-1α), suppressed oxidative stress marker (malondialdehyde), enhanced antioxidant defence mechanisms (reduced glutathione and glutathione peroxidase), a modulated inflammatory response [interleukin-6 (IL-6), monocyte chemoattractant protein-1, IL-10 and α-7-nicotinic acetylcholine receptor) and ameliorated angiogenic regulators [matrix metalloproteinase (MMP-2), MMP-9 and tissue inhibitor of metalloproteinase-1), as well as the tissue damage indicator (lactate dehydrogenase) in organ tissues. In addition, there were significant improvement in serum inflammatory markers tumour necrosis factor-α, IL-10, IL-1β and C-reactive protein compared with irradiated mice. The histopathological investigation of the FX + RAD organ tissues support the biochemical findings where the improvements in the tissues’ architecture were obvious when compared with those of RAD. FX was thus shown to have a noticeable radioprotective action mediated through its regulatory effect on the apelin-13/APJ/NF-κB signalling pathway attributed to its antioxidant and anti-inflammatory activity that was reflected in different physiological processes. It could be recommended to use FX in cases of radiation exposure to protect normal tissues.

Dietary inclusion of non-conventional palm kernel meal enhances growth, digestive enzyme activities and carcass characteristics of juvenile rohu (Labeo rohita)

A 60-day feeding trial was performed to test the nutritional value and utilization possibility of palm kernel meal (PKM) as a feed ingredient for juvenile Labeo rohita. Five iso-nitrogenous diets were prepared with various inclusions of PKM which replaced sunflower oil cake and de-oiled rice bran namely, control (without PKM), T1 (50 g/kg PKM), T2 (100 g/kg PKM), T3 (150 g/kg PKM) and T4 (200 g/kg PKM). The experiment was conducted in 350 L fibre reinforced plastic tanks in triplicate and each tank stocked with twenty-five juvenile rohu (7.2 ± 0.01 g) were fed twice daily at 5% of body weight with the experimental diet. The growth performance values showed a higher overall linear trend in T2 and it is significantly different from control as well as T1 groups. Final results showed highest average body weight, specific growth rate, protein efficiency ratio, and apparent net protein utilization in a dose-dependent manner (p < 0.05). Significantly higher amylase, protease, and lipase activities were recorded in T2 treatment (p = 0.003, p = 0.001 and p = 0.002, respectively). Additionally, dietary PKM significantly lowered the aspartate amino transferase, alkaline amino transferase and alkaline phosphatase enzyme activities in a dose-dependent manner (p < 0.05). Significantly higher lactate dehydrogenase, malate dehydrogenase, superoxide dismutase and catalase activities in the liver tissues were recorded in T4 (p = 0.004, p = 0.01 and p = 0.02 and p = 0.001, respectively). Based on the polynomial regression analysis, the PKM inclusion at 26.17–100.11 g/kg can be effectively used in the diet of juvenile L. rohita as a non-conventional growth-promoting feed ingredient without any harmful effects on its growth performance and physiological activities.

Glutathione reductase and catalase as potential biomarkers for synergistic intoxication of pesticides in fish

Synergy occurs when chemicals give pronounced effect on combination in contrast to their individual effect. The objective of this study was to investigate the synergistic effect of pesticides carbaryl (C) and methyl parathion (MP) on oxidative stress biomarkers viz catalase (CAT), glutathione reductase (GSSG-R) including different enzymes like lactate dehydrogenase (LDH), succinate dehydrogenase (SDH) and acetyl cholinesterase (AChE) in different tissues of carps Catla catla. Fishes were exposed to 6.25 mg/L of MP and 2.3 mg/L of C in mixture (one-third of LC50 value). CAT and GSSG-R were studied in gills, brain, liver and muscle of carp were found to be elevated significantly (p < 0.005). LDH activity increased significantly (p < 0.005) in synergistic group, there was a seven-fold (748%) increase in LDH activity in muscle compared to individual studies with same pesticides. Contrary to LDH, sudden decrease in SDH activity was accounted. Significant (p < 0.005) decrease in AChE activity after initial 24 h was remarkable addressing to the shift in neurotransmission pathway in organism. Significant increase was observed in activity of CAT and GSSG-R in all tissues compared to control fishes in individual as well as synergistic (MP + C) group suggesting that CAT and GSSG-R can be a potential biomarker of oxidative stress when studied in combination.

Response of AMP-activated protein kinase and lactate metabolism of largemouth bass (Micropterus salmoides) under acute hypoxic stress

To study adaptation of largemouth bass (Micropterus salmoides) to hypoxic stress, we investigated physiological responses and lactate metabolism of the fish under acute hypoxia. The objectives of this study were to (a) observe changes in glucose, glycogen, and lactate content; (b) detect the activity of lactate dehydrogenase (LDH) in serum, brain, heart, and liver tissues; and (c) quantify the dynamic gene expression of AMP activated protein kinase alpha (AMPKα), hypoxia-inducible factor-1 alpha (HIF-1α), monocarboxylate transporter 1 (MCT1), monocarboxylate transporter 4 (MCT4), and lactate dehydrogenase-a (LDHa) following exposure to hypoxia. The fish were subjected to two hypoxia stresses (dissolved oxygen [DO] 1.20 ± 0.2 mg/L and 3.50 ± 0.3 mg/L, respectively) for 24 h. Our results showed that hypoxic stress significantly increased the decomposition of liver glycogen and significantly increased the concentration of blood glucose; however, the muscle glycogen content was not significantly decreased, which indicates that liver glycogen was the main energy source under acute hypoxia. Moreover, hypoxia led to accumulation of a large amount of lactic acid in tissues, possibly due to the activity of lactic acid dehydrogenase, but this process was delayed in the heart and brain relative to the liver. Additionally, hypoxia induced the expression of AMPKα, HIF-1α, MCT1, MCT4, and LDHa, suggesting that glycometabolism had switched from aerobic to anaerobic. Our results contribute to a better understanding of the molecular mechanisms of the response to hypoxia in largemouth bass.

Double-stranded RNA-dependent kinase PKR activates NF-κB pathway in acute pancreatitis

The activation of transcription factor nuclear factor kappa B (NF-κB) occurs early in acute pancreatitis (AP) simultaneously with intracellular trypsinogen activation. Double-stranded RNA-dependent kinase (PKR) promotes the activation of NF-κB and the production of pro-inflammatory factors including tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6). The rat and rat pancreatic AR42J cells were treated by cerulein to establish AP models, showing PKR increased. TNF-α, IL-6 and lactate dehydrogenase (LDH) in AP pancreatic tissues and cerulein-treated AR42J cells increased, while PKR knockdown in AR42J cells reversed cerulein-induced inflammatory response and pancreatic cell injury. In addition, inhibitor of kappa B kinase α (IKKα), phosphorylated P65 (p-P65), P65 increased in cerulein-treated AR42J cells. Meanwhile, in cerulein-treated AR42J cells, interaction between PKR and IKKα, as well as the co-localization and nuclear accumulation of PKR and P65, were detected. Furthermore, cerulein induced the phosphorylation and nuclear translocation of P65, which indicated the activation of NF-κB, while PKR knockdown hindered NF-κB activation to alleviate pancreatic cell injury. In summary, PKR might promote NF-κB activation via facilitating its phosphorylation and nuclear translocation, thus accelerated inflammatory response and pancreatic cell injury in AP, implying a novel molecular target for the treatment of AP.

Protective Effect of Kolaviron on Cyclophosphamide-Induced Cardiac Toxicity in Rats.

Background.Cyclophosphamide (CP) is a nitrogen mustard alkylating drug used for the treatment of chronic and acute malignant lymphomas, myeloma, leukemia, neuroblastoma, adenocarcinoma, retinoblastoma, breast carcinoma, and immunosuppressive therapy. Despite its vast therapeutic uses, it is known to cause severe cardiac toxicity. Kolaviron (KV), a Garcinia kola seed extract containing a mixture of flavonoids, is reputed for its antioxidant and membrane stabilizing properties.Objective.This study investigated the protective effect of KV on CP-induced cardiotoxicity in rats.Methods.Thirty rats were used, and they were divided into 6 groups of 5 rats each. Group I received 2 mL/kg propylene glycol orally for 14 days; group II received CP (50 mg/kg/d, intraperitoneally [i.p.]) for 3 days; groups III and IV received 200 and 400 mg/kg/d KV, respectively, orally for 14 days and groups V and VI were pretreated with 200 and 400 mg/kg/d KV, respectively, orally for 14 days followed by CP (50 mg/kg/d, i.p.) for 3 days.Results.CP treatment resulted in a significantly lower food consumption and body weight in rats. The lactate dehydrogenase and creatine kinase enzymes in cardiac tissues of rats treated with CP were significantly higher. In cardiac tissues, 3-day doses of CP resulted in significantly higher heart weight, cardiac troponin I, myeloperoxidase, malondialdehyde, hydrogen peroxide and lower superoxide dismutase, catalase, glutathione peroxidase activities, and reduced glutathione levels. Histological examination of cardiac tissues showed sign of necrosis of myocardium after CP treatment. However, administration of KV at 200 and 400 mg/kg for 14 days prior to CP treatment, increase food consumption, body weight, and attenuates the biochemical and histological changes induced by CP.Conclusions.These results revealed that KV attenuates CP-induced cardiotoxicity by inhibiting oxidative stress and preserving the activity of antioxidant enzymes.

Ergosterol Attenuates LPS-Induced Myocardial Injury by Modulating Oxidative Stress and Apoptosis in Rats

Background/Aims: Ergosterol (ER) is the primary sterol found in fungi and is named after the ergot fungus. A variety of pharmacological activities have been reported for ER, including antioxidative, anti-proliferative, and anti-inflammatory effects, although its role in sepsis remains unclear. Methods: The protective effect of ER on lipopolysaccharide (LPS)-induced sepsis myocardial injury was evaluated both in vivo and in vitro. Rats were pretreated with ER and then with LPS. Histopathology of heart tissues was first performed. Subsequently, the levels of superoxide dismutase (SOD), malondialdehyde (MDA), creatine kinase MB fraction (CK-MB), and lactate dehydrogenase (LDH) in serum and heart tissues were assessed by enzyme-linked immunosorbent assay kits. Western blotting was further used to evaluate the expression of antioxidant proteins (HO-1 and cytochrome c) and apoptosis associated proteins (Bcl-2, Bax, cleaved-caspase-3, cleaved-caspase-9, and cleaved-PARP). In addition, the effects of ER on oxidative stress biomarkers and apoptosis proteins were also detected in LPS-treated H9C2 cells. Moreover, small interfering Nrf2 RNA was transfected to H9C2 cells to study the role of Nrf2 signaling in connection with the protective effects of ER. Results: Pretreatment with ER ameliorated the histopathological changes in heart tissue induced by LPS injection, increased SOD activity, and reduced MDA content, and CK-MB and LDH levels. Furthermore, ER restored the expression of Nrf-2 and HO-1 in rat hearts, attenuating apoptotic damage via up-regulation of Bcl-2 in combination with the inhibition of Bax, cytochrome c, cleaved-caspase-3 and 9, and PARP, as revealed by western blot. When Nrf2 was blocked by siRNA, the effects of ER on SOD and MDA activity, as well as the expression of the antioxidant proteins and apoptosis-associated proteins were abolished. Conclusions: We demonstrated that ER has a cardioprotective effect in LPS-induced sepsis model through modulation of the antioxidant activity and anti-apoptosis effects and this process might be regulated by Nrf2 signaling.

Curcumin mediated attenuation of carbofuran induced toxicity in the heart of Wistar rats.

Carbofuran is used to improve the agricultural productivity as well as to protect the house hold and industrial products, but due to accumulation in the biological system, it causes serious side effects in many non-targets mammalian systems. The aim of present study is to evaluate the carbofuran induced oxidative stress in rat heart and its attenuation by using herbal product curcumin. Rats were divided into four groups; one group received 20 % LD50 of carbofuran another group of rats received same doses of carbofuran was pretreated with curcumin (100 mg kg-1 body weight) and remaining two other groups served as control and curcumin treated animals. The activity of lactate dehydrogenase (LDH) in the heart tissues and serum was evaluated and the activity of enzymatic antioxidants superoxide dismutase (SOD) and catalase (CAT) was estimated in the heart tissues. The level of malondialdehyde (MDA) in heart tissues was also measured. The Total cholesterol (TC) and high density lipoprotein (HDL) was measured in the serum of the entire animals group. The results of present study showed that the activity of LDH in heart tissues were decreased and in serum was elevated. The MDA level was significantly elevated due to exposure of carbofuran. The enzymatic antioxidants, SOD and CAT activities were also inhibited. The ratio of pro-oxidant (P)/antioxidant (A) was also found to be sharply increased in the rat heart tissues of carbofuran exposed animals. The alterations in all the parameter were recovered by the pretreatment of curcumin (100 mg kg-1 body weight).

The Protective Effects of Helix B Surface Peptide on Experimental Acute Liver Injury Induced by Carbon Tetrachloride.

To investigate the protective effects of helix B surface peptide (HBSP) on acute liver injury induced by carbon tetrachloride (CCl4). HBSP (8nmol/kg) was intraperitoneally injected into C57 BL/6 mice 2h after CCl4 administration. Serum and liver tissue samples were collected 24h after injury. Liver function and histological injuries were evaluated. Inflammatory cell infiltration and cytokines were examined and hepatocytes apoptosis was measured. The human liver cell line LO2 and murine primary hepatocytes were stimulated by CCl4 with and without HBSP treatment and glutathione peroxidase activity, cell survival, and apoptosis were evaluated. In addition, we examined the PI3K/Akt/mTORC1 pathway to elucidate the mechanism underlying HBSP-mediated protection in acute liver injury. HBSP significantly decreased serum alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and pro-inflammatory cytokines in liver tissues after CCl4 injection compared with those in the control group. Immunohistochemical staining indicated that the number of CD3-, CD8-, and CD68-positive cells and the expression of cleaved caspase-3 were significantly decreased by HBSP treatment. Additionally, HBSP reduced apoptosis in vivo. In an in vitro study, the glutathione peroxidase activity and survival rate increased, while the total apoptotic rate was reduced in the HBSP-treated group compared with that in the control group after CCl4 treatment. HBSP activated the PI3K/Akt/mTORC1 pathway, which was confirmed by the PI3K inhibitor LY294002 both in vivo and in vitro. Furthermore, HBSP increased the survival of mice with acute liver injury, and this effect was abolished by LY294002. HBSP is a potential therapeutic agent against acute liver injury induced by CCl4.

Protective Effect of Curcumin Against Carbofuran-Induced Toxicity in Wistar Rats.

Pesticide carbofuran (Furadan) is known to be an inhibitor of nerve impulses by its inhibition of acetylcholinesterase. Oral administration of carbofuran also produced tissue damage as evidenced by the increased the activities of creatine kinase (CK), lactate dehydrogenase (LDH), and gamma glutamyl transferase (γ-GT) in tissues and serum. Against carbofuran, curcumin restored the activities of acetylcholinesterase, LDH, CK and γ- GT in animals. Curcumin also restored the reduced mitochondrial enzymes in rat liver caused by carbofuran. Liver carbohydrate metabolizing enzyme hexokinase was increased, and glucose 6-phosphate dehydrogenase, fructose 1,6 diphosphatase, and glucose 6-phosphatase decreased after carbofuran treatment. Treatment with curcumin improved these enzyme activities in the liver. Carbofuran exposure resulted in increased lipid peroxidation (LPO), hydroperoxides, and conjugated diene in liver. Administration of curcumin during carbofuran administration lowered LPO, conjugated diene, and hydroperoxides. Moreover, levels of superoxide dismutase, glutathione peroxidase, catalase, and glutathione, which were significantly decreased after carbofuran exposure, were increased by curcumin administration. Marked impairment in the motor function was seen following carbofuran administration. Curcumin treatment significantly improved the carbofuran-induced neurobehavioral difficulties. These results indicate the ameliorating activity of carbofuran toxicity by curcumin.

Isoenzyme spectra of lactate dehydrogenase in tissues of mammals of the Mustelidae family

A comparative analysis of distribution of lactate dehydrogenase (LDH) isoenzymes in the heart, kidneys, lungs, spleen, liver and skeletal muscle was performed in 4 species of carnivorous mammals (Mustelidae family): American mink (Mustela vison Schr.), polecat (Mustela putorius L.), sable (Martes zibellina L.) and pine marten (Martes martes L.). It was found that in the mink, unlike pure terrestrial mustelids (polecat, sable, pine marten), the anaerobic LDH-5 fraction was predominant in the LDH isoenzyme spectrum in the liver, skeletal muscle, lungs and spleen. In all species studied, aerobic B(H) subunits of LDH were found to prevail in the heart and kidney, whereas anaerobic A(M) subunits prevailed in the liver and spleen. The tissue- and species-specific features of LDH isoenzyme spectra revealed in different mustelids reflect the biochemical adaptation of the animals to environmental conditions.

The isozyme spectra of lactate dehydrogenase in the tissues of the raccoon dog Nyctereutes procyonoides in the autumn

An electrophoretic assay of lactate dehydrogenase (EC 1.1.1.27) isozymes in the tissue homogenates of cardiac and skeletal muscles, kidney, lungs, spleen, and liver of the raccoon dog Nyctereutes procyonoides from two different geographic zones, viz., northwestern Russia and Poland, as well as the Arctic blue fox Alopex lagopus L. and the red fox Vulpes vulpes L. was performed during the preparatory period to the winter season. Raccoon dogs, which hibernate under natural conditions, differ from other canids (the red fox and Arctic blue fox) to which they are close taxonomically by their body weight and by the higher proportion of aerobic H subunits of lactate dehydrogenase in all organs except for the heart. A higher content of “fast” anode fractions, lactate dehydrogenase-1 and lactate dehydrogenase-2, in the heart, kidney, lungs, liver, and spleen was detected in the raccoon dogs from the northern region compared to those from the southern geographic zone. The shift in the reaction catalyzed by lactate dehydrogenase towards the production of pyruvate indicates that this metabolite is necessary for the synthesis of fatty acids during lipogenesis in the autumn.

기아상태에서 Ldh-C가 발현된 어류 조직의 젖산탈수소효소의 대사

기아상태에서 Ldh-C가 발현된 어류 조직의 젖산탈수소효소의 대사

Dioscorea bulbifera polysaccharide and cyclophosphamide combination enhances anti-cervical cancer effect and attenuates immunosuppression and oxidative stress in mice.

Cyclophosphamide (CTX) is commonly used in cancer chemotherapy, which causes immunosuppression and tissue oxidative stress at high doses. As potential protective agents, some polysaccharides were shown to have anti-tumor, anti-inflammatory and/or anti-oxidant properties. This study explored potential effects of oral treatment of Dioscorea bulbifera polysaccharides (DBLP at 100 or 150 mg/kg) in U14 cervical tumor-bearing mice treated with CTX (25 mg/kg). While CTX suppressed tumor growth (65.4% inhibition) and DBLP alone also inhibited tumor (25.6% at 100 mg/kg or 37.6% at 150 mg/kg), CTX+DBLP combination produced tumor inhibition rates of 5.6 (for 100 mg/kg DBLP) or 9% (for 150 mg/kg) higher than CTX alone. While tumor itself and CTX treatment reduced thymus and/or spleen/body weight indices, DBLP alone or CTX + DBLP combination attenuated this reduction. DBLP lowered peripheral blood T-cell subpopulation CD4+/CD8+ ratio, and DBLP+CTX combination attenuated CTX effect in lifting CD4+/CD8+ ratio. Tumor itself and CTX treatment heightened oxidative stress (with decreased superoxide dismutase but increased lactate dehydrogenase and malondialdehyde levels in serum and tissues), which was attenuated by DBLP treatment, and DBLP+CTX combination suppressed CTX-induced oxidative stress. Combination use of DBLP with CTX can potentially enhance CTX anti-tumor effect and can attenuate CTX-induced immunosuppression and oxidative stress in U14 cervical tumor-bearing mice.