Lactate Dehydrogenase Activity Levels Research Articles

Habitat pollution and thermal regime modify molecular stress responses to elevated temperature in freshwater mussels (Anodonta anatina: Unionidae)

Elevated temperature and pollution are common stressors in freshwater ecosystems. We study cellular stress response to acute warming in Anodonta anatina (Unionidae) from sites with different thermal regimes and pollution levels: a pristine area and an agriculturally polluted site with normal temperature regimes (F and A, respectively) and a polluted site with elevated temperature (N) from the cooling pond of an electrical power plant. Animals were exposed to different temperatures for 14days and stress response markers were measured in gills, digestive gland and hemocytes. Mussels from site N and A had elevated background levels of lactate dehydrogenase activity indicating higher reliance on anaerobic metabolism for ATP production and/or redox maintenance. Exposure to 25°C and 30°C induced oxidative stress (indicated by elevated levels of lipid peroxidation products) in digestive gland and gills of mussels from A and F sites, while in mussels from N sites elevated oxidative stress was only apparent at 30°C. Temperature-induced changes in levels of antioxidants (superoxide dismutase, metallothioneins and glutathione) were tissue- and population-specific. Acute warming led to destabilization of lysosomal membranes and increased frequencies of nuclear lesions in mussels from F and A sites but not in their counterparts from N site. Elevated temperature led to an increase in the frequency of micronuclei in hemocytes in mussels from F and A sites at 25°C and 30°C and in mussels from N site at 30°C. The mussels from N site also demonstrated better survival at elevated temperature (30°C) than their counterparts from the F and A sites. Taken together, these data indicate that long-term acclimation and/or adaptation of A. anatina to elevated temperatures result in increased thermotolerance and alleviate stress response to moderate temperature rise. In contrast, extreme warming (30°C) is harmful to mussels from all populations indicating limit to this induced thermotolerance.

Ellagic acid-induced thrombotic focal cerebral ischemic model in rats

IntroductionIschemic stroke is a common cause of human disability and death. Animal models of focal cerebral ischemia are widely utilized to mimic human ischemic stroke. Although models of focal cerebral ischemia have been well established, very few evidence is based on triggering the intrinsic coagulation system to induce focal cerebral ischemia. Ellagic acid (EA) has been identified to trigger the intrinsic coagulation system via activating coagulation factor XII. However, it remains unknown whether EA can serve as a novel pharmacological approach to induce a new model of focal cerebral ischemia in rats. MethodsEA was used for inducing focal cerebral ischemia in adult rats. The dose- and time-dependent effects of EA were characterized. The cerebral infarction ratio was determined with triphenyltetrazolium chloride staining, and the histopathological analysis of the brain tissue was performed under light microscopy. The neurological deficit score was evaluated by a modified method of Bederson. Malondialdehyde (MDA) level and lactate dehydrogenase (LDH) and superoxide dismutase (SOD) activities in serum were determined by spectrophotometry. ResultsInjection of EA into the middle cerebral artery of rats was able to generate focal cerebral infarction and increased the neurological deficit score and the brain weight to body weight ratio in dose- and time-dependent manners. Furthermore, EA raised serum LDH activity and MDA level and decreased serum SOD activity in a dose-related fashion. DiscussionThis is the first evidence to show that EA induces focal cerebral ischemia in rats, which is similar to human ischemia stroke in pathogenesis. This model holds promise for pathological, pharmacological and clinical studies of ischemic stroke.

Protective effect of NMDA receptor antagonist memantine on acute lung injury in mice

To investigate the protective effect of a non-specific NMDA receptor antagonist memantine on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Healthy male mice were divided into 4 groups: a normal group, a memantine group, an ALI group and a memantine+ALI group. The ALI group was induced by intraperitoneal injection of LPS (10 mg/kg). Memantine (10 mg/kg) was injected intraperitoneally before the injection of LPS to determine the effect of blockade of NMDA receptor in the memantine+ALI group. The lung wet/dry ratio was detected. HE staining was preformed to show the morphological changes in the lung tissue. Myeloperoxidase enzyme (MPO) activity and malondialdehyde (MDA) content in the lung tissue were detected. ELISA was used to detect the tumor necrosis factor-α (TNF-α) content and lactate dehydrogenase (LDH) activity in the bronchoalveolar lavage fluid (BALF). Memantine pretreatment improved the LPS-induced ALI lung tissue morphological changes, reduced their lung wet/dry ratio, the levels of TNF-α and LDH activity in BALF, and also reduced the MPO and MDA content in the lung tissue. Blockade of NMDA receptors can ameliorate LPS-induced mice ALI.

Impact of Agrimin And Fishmin on the Carbohydrate Metabolic Enzymes in the Muscle and Liver Tissue of the Different Fish (C.Catla. L. Rohita. C.Mrigala) Species

The present study is aimed at investigating the effect of selective Synthetic feed like Agrimin and Fishmin on carbohydrate metabolic enzymes of the cultivable fish species like Catla catla, Labeo rohita, Cirrhinus mrigala. The fishes selected for the study shall be divided into two groups viz. control group and experimental group age two years .The control group of fishes shall be fed with control feed i.e. Groundnut cake, rice bran. The experimental group of fishes shall further be divided into two groups. Agrimin and Fishmin which are commercially available. have been selected for the study. The first group of experimental fish shall be fed with control feed mixed with Agrimin. The second group of experimental fish shall be fed with control feed mixed with fishmin. The two groups of experimental fish shall be fed twice a day at 10 a.m. and at 5 p.m. The exposure period selected for the study is 30 days after 30 days the fishes were killed and isolated the tissues like muscle and liver at 4 0 C and assayed the activity of Aldolose. MDH (Malate dehydrogenase). SDH (Succinate dehydrogenase) and LDH (Lactate dehydrogenase). Agrimin and fishmin enhanced the various fish species muscle and liver tissues enzymes such as Aldolose, MDH, SDH and LDH activity levels.

Critical role of Th17 cells in development of autoimmune hemolytic anemia

Autoimmune hemolytic anemia (AIHA) is defined as the increased destruction of red blood cells (RBCs) in the presence of anti-RBC autoantibodies with or without complement activation. However, the underlying mechanism for the development of AIHA remains largely unclear. In this study, we carefully evaluated the potential role of Th17 cells in the development of AIHA. We found an elevated frequency of Th17 cells in patients with AIHA, which were closely correlated with their disease activity, including the level of anti-RBC IgG antibodies, hemoglobin, serum C3, and lactate dehydrogenase activity. Furthermore, we observed that interleukin (IL)-17 was also closely correlated with the disease activity in AIHA patients. To further elucidate the potential role of Th17 cells in induction of AIHA, we used the Marshall-Clarke and Playfair model of murine AIHA. Notably, we found that Th17 cells affected development of AIHA by enhancing the adaptive humoral responses. Specifically, we found that adoptive transfer of Th17 cells heightened the initial anti-rat RBC antibody responses and concomitantly increased the onset of AIHA. In addition, invivo neutralization of IL-17 abrogated the development of AIHA, while initiation of anti-rat RBC IgG responses and induction of AIHA in IL-17(-/-) mice were impaired. Our findings suggest that Th17 cells contribute to the development of AIHA, which could facilitate our better understanding of AIHA pathogenesis and provide clues to developing novel forms of immunotherapy against AIHA.

Altered Prion Protein Expression Pattern in CSF as a Biomarker for Creutzfeldt-Jakob Disease

Creutzfeldt-Jakob disease (CJD) is the most frequent human Prion-related disorder (PrD). The detection of 14-3-3 protein in the cerebrospinal fluid (CSF) is used as a molecular diagnostic criterion for patients clinically compatible with CJD. However, there is a pressing need for the identification of new reliable disease biomarkers. The pathological mechanisms leading to accumulation of 14-3-3 protein in CSF are not fully understood, however neuronal loss followed by cell lysis is assumed to cause the increase in 14-3-3 levels, which also occurs in conditions such as brain ischemia. Here we investigated the relation between the levels of 14-3-3 protein, Lactate dehydrogenase (LDH) activity and expression of the prion protein (PrP) in CSF of sporadic and familial CJD cases. Unexpectedly, we found normal levels of LDH activity in CJD cases with moderate levels of 14-3-3 protein. Increased LDH activity was only observed in a percentage of the CSF samples that also exhibited high 14-3-3 levels. Analysis of the PrP expression pattern in CSF revealed a reduction in PrP levels in all CJD cases, as well as marked changes in its glycosylation pattern. PrP present in CSF of CJD cases was sensitive to proteases. The alterations in PrP expression observed in CJD cases were not detected in other pathologies affecting the nervous system, including cases of dementia and tropical spastic paraparesis/HTLV-1 associated myelopathy (HAM/TSP). Time course analysis in several CJD patients revealed that 14-3-3 levels in CSF are dynamic and show a high degree of variability during the end stage of the disease. Post-mortem analysis of brain tissue also indicated that 14-3-3 protein is upregulated in neuronal cells, suggesting that its expression is modulated during the course of the disease. These results suggest that a combined analysis of 14-3-3 and PrP expression pattern in CSF is a reliable biomarker to confirm the clinical diagnosis of CJD patients and follow disease progression.

Changes of selected biochemical indicators and electrocardiography indicators in nutritional muscular dystrophy in calves

The aim of this study was to estimate changes in selected biochemical indicators during nutritional muscular dystrophy of calves and to use electrocardiography technique in early diagnosis of this disease. The study was performed on 24 Holstein-Friesian calves of both sexes, divided into two groups. The first one was experimental group of 12 calves with symptoms of nutritional muscular dystrophy and the second one was control group of 12 clinically healthy calves administered a single i.m. injection of vitamin E + selenium preparation on the second day after birth. Blood samples were collected from all animals 3 × at 7-day intervals, starting on day 5. Blood serum was subjected to biochemical analyses to determine Se and vitamin E concentrations, aspartate aminotransferase, creatine kinase and lactate dehydrogenase activity levels. The activity of glutathione peroxidase was determined in whole blood samples. Electrocardiographic assessment was performed on day 19 in all calves. In the group of calves with symptoms of nutritional muscular dystrophy, serum Se and vitamin E concentrations were significantly (P ≤ 0.01) lower than in control, the same was true for the activity of glutathione peroxidase (P ≤ 0.01). The changes were accompanied by an increase (P ≤ 0.01) in the activity of aspartate aminotransferase, creatine kinase and lactate dehydrogenase. The electrocardiograms of experimental animals revealed elevated heart rate, accelerated sinus rhythm, increased P wave amplitude, shorter PR, QT and ST interval, narrower QRS complex, shorter T wave duration and insignificantly increased T wave amplitude; these results were indicative of arrhythmia which is observed at early stages of cardiomyopathy. This study is the first one in which electrocardiography technique was used to diagnose nutritional muscular dystrophy in calves.

Flower extract of Nyctanthes arbor-tristis modulates glutathione level in hydrogen peroxide treated lymphocytes

Background:Nyctanthes arbor-tristis Linn (Oleaceae) is a well-known traditional medicinal plant used throughout the India as an herbal remedy for treating various infectious and non-infectious diseases.Objective:To evaluate the antioxidative activity of hydro-alcoholic extract of flower in the lymphocytes exposed to oxidative stress induced by H2O2 .Materials and Methods:Isolated lymphocytes were treated in vitro with extract or extract+H2O2, and the level of reduced glutathione (GSH) as well as the activity of glutathione-S-transferase (GST) and lactate dehydrogenase (LDH) were measured.Results:Treatment of lymphocyte with flower extract (50, 100, and 200 μg/ ml) significantly increased the level of GSH and decreased the activity of GST. The LDH activity measured in the cell-free medium decreased significantly. Pre-treatment of lymphocyte with flower extract protects the lymphocyte from the H2O2 induced oxidative stress by significantly increasing the levels of GSH as compared to the cells treated only with H2O2. Pre-treatment also reduced the activity of LDH significantly as compared to the cells treated only with H2O2. The LDH activity in cell-free medium is associated with membrane damage, the decreased levels of LDH activity reflects the reduced level of membrane damage due to H2O2.Conclusion:The present findings suggest the protective role of the hydro-alcoholic extracts of the flower of Nyctanthes arbor-tristis against membrane damage induced by H2O2. The results also suggest that the extract might be rich in phytochemicals with antioxidant/radical scavenging potentials, which might find application in antioxidant therapy.

Effect of maternal exposure to ozone on reproductive outcome and immune, inflammatory, and allergic responses in the offspring

There is growing concern that exposure to air pollutants during pregnancy affects health outcomes in the offspring due to alterations in the development of immune and other homeostatic processes. To assess the risks of maternal inhalation exposure to ozone (O3), timed pregnant BALB/c mice were exposed to different concentrations of O3 (0, 0.4, 0.8, and 1.2 ppm) for 4 h/day for 10 days during gestation (GD9–GD18), and pulmonary inflammation and immune responses were assessed in the offspring at 6 weeks-of-age. Maternal O3 exposure reduced the number of productive dams by 25% at the highest O3 concentration (1.2 ppm) and decreased the rate of weight gain in the offspring. Delayed-type hypersensitivity responses to bovine serum albumin were suppressed in the female offspring by maternal exposure to the two highest concentrations of O3, whereas humoral immune responses to sheep red blood cells were not altered in either sex. Maternal exposure to 1.2 ppm O3 increased lactate dehydrogenase (LDH) activity in bronchoalveolar lavage fluid (BALF) of the offspring but did not affect the number of inflammatory cells or levels of total protein, IFN-γ, IL-17, and IL-4 cytokines in BALF, or CD4+, CD8+, CD25+, and TCRβ+CD1d+ T-cells in the spleen. Offspring born from air-exposed dams sensitized early in life (postnatal day [PND] 3) to ovalbumin (OVA) antigen and then challenged as adults developed eosinophilia, elevated levels of LDH activity and total protein in BALF, and increased pulmonary responsiveness to methacholine, compared with animals sensitized at PND42. Maternal O3 exposure in the 1.2 ppm O3 group decreased BALF eosinophilia and serum OVA-specific IgE in the female offspring sensitized early in life but did not affect development of allergic airway inflammation by offspring sensitized late in life. In summary, maternal exposure to O3 affected reproductive outcome and produced modest decreases in immune function and indicators of allergic lung disease in surviving offspring.

Effects of long-term silymarin oral supplementation on the blood biochemical profile of rainbow trout (Oncorhynchus mykiss)

Silymarin, an extract from "milk thistle" (Silybum marianum) plant is traditionally used as herbal medicine. The present study was conducted to investigate the clinical effects and possible side effects of silymarin on biochemical blood parameters of rainbow trout (Oncorhynchus mykiss). Fishes were treated with 0 (control), 100, 400, and 800 mg of silymarin per kg of food during 4 weeks. Plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), creatine kinase (CK), glucose, total protein, creatinine, triglyceride, cholesterol, urea, uric acid and liver cellular total antioxidant, and protein content were measured after 7, 14, and 28 days of silymarin treatment. The results showed that oral administration of silymarin in fish significantly reduced plasma glucose and cholesterol levels and relatively increased plasma total protein and globulin concentrations (P < 0.05). Increasing plasma albumin levels indicate the important role of albumin in drug transportation in circulatory system of fish. Silymarin also stabilized cellular membrane structure and regulated the levels of AST, ALT, ALP, CK, and LDH activity. In conclusion, on the basis of these results, oral administration of silymarin up to 400 mg per 1 kg of food has no side effect on blood biochemical and clinical parameters of fishes. However, oral administration of 800 mg/kg- of silymarin caused cytotoxicity and modifications in blood biochemical parameters of fish.

Effects of Caulophine on Caffeine‐induced Cellular Injury and Calcium Homeostasis in Rat Cardiomyocytes

Caulophine is a novel fluorenone alkaloid isolated from the radix of Caulophyllum robustum Maxim. Caulophine showed high affinity for the rat myocardial cell membrane as assessed by cell membrane chromatography, suggesting that the compound may exert bioactivity in the heart. It is known that calcium plays an important role in the pathogenesis of ischaemic heart disease, and caffeine can cause calcium overload in cardiomyocytes by inducing calcium release from the sarcoplasmic reticulum. Therefore, the present study evaluated the effects of caulophine on caffeine-induced injury and calcium homeostasis in cardiomyocytes. Cardiomyocytes were pre-treated with caulophine before exposure to caffeine or potassium chloride (KCl). Cell viability was assayed using the MTT method, and lactate dehydrogenase (LDH) and malondialdehyde (MDA) were measured spectrophotometrically. Caulophine-pre-treated cardiomyocytes were incubated with Fluo-3/AM, and then caffeine or KCl was used to induce Ca(2+) overload. The total intracellular Ca(2+) concentration was measured by flow cytometry. Fluorescence densities of single cardiomyocytes were detected using a confocal microscope. Caulophine increased the viability of caffeine-injured cardiomyocytes and decreased LDH activity and MDA level in cardiomyocytes. Furthermore, caulophine significantly decreased the total intracellular free Ca(2+) concentration and intracellular calcium release in cardiomyocytes in response to caffeine. However, the same concentrations of caulophine did not affect KCl-induced calcium influx. Our results suggest that caulophine protects cardiomyocytes from caffeine-induced injury as a result of calcium antagonism. This finding provides a basis for further study and development of caulophine as a new calcium antagonist for treating ischaemic cardiovascular diseases.

Interaction between chronic arsenic exposure via drinking water and plasma lactate dehydrogenase activity

Arsenic is a potent environmental pollutant that has caused one of the largest public health poisonings in the history of human civilization, affecting tens of millions of people worldwide especially in Bangladesh. Lactate dehydrogenase (LDH) in blood plays an important role in predicting cell or organ damage and as an important clue to the diagnosis of a variety of cancers. However, effect of chronic arsenic exposure on the LDH level in blood has not yet been documented. Since the chronic arsenic exposure is associated with organ damages and multi-site cancers, this research aimed at assaying the plasma level of LDH activity in the population who were exposed to arsenic chronically in Bangladesh. A total of 185 individuals living in arsenic-exposed areas and 121 individuals living in non-exposed area in Bangladesh were recruited as study subjects. Arsenic content in drinking water, hair and nails were estimated by Inductively Coupled Plasma Mass Spectroscopy (ICP-MS) and LDH activity was assayed by a spectrophotometer. Significant increase in LDH activity was observed with increasing concentrations of arsenic in water, hair and nails. Further, the study subjects were split into four groups based on the three ways of each exposure metrics (water, hair and nail arsenic concentrations) where the study subjects in the non-exposed area were used as a reference (lowest exposure) group. LDH activity was found to be increased in the higher exposure groups of water and hair arsenic concentrations. LDH activity was also increased at low to medium exposure groups of nail arsenic concentrations.Thus, the elevated plasma LDH activity might be helpful for the early prognosis of organ or tissue damage in the individuals who were exposed to arsenic chronically.

Mechanism of De Novo Branched-Chain Amino Acid Synthesis as an Alternative Electron Sink in Hypoxic Aspergillus nidulans Cells

Although branched-chain amino acids are synthesized as building blocks of proteins, we found that the fungus Aspergillus nidulans excretes them into the culture medium under hypoxia. The transcription of predicted genes for synthesizing branched-chain amino acids was upregulated by hypoxia. A knockout strain of the gene encoding the large subunit of acetohydroxy acid synthase (AHAS), which catalyzes the initial reaction of the synthesis, required branched-chain amino acids for growth and excreted very little of them. Pyruvate, a substrate for AHAS, increased the amount of hypoxic excretion in the wild-type strain. These results indicated that the fungus responds to hypoxia by synthesizing branched-chain amino acids via a de novo mechanism. We also found that the small subunit of AHAS regulated hypoxic branched-chain amino acid production as well as cellular AHAS activity. The AHAS knockout resulted in higher ratios of NADH/NAD(+) and NADPH/NADP(+) under hypoxia, indicating that the branched-chain amino acid synthesis contributed to NAD(+) and NADP(+) regeneration. The production of branched-chain amino acids and the hypoxic induction of involved genes were partly repressed in the presence of glucose, where cells produced ethanol and lactate and increased levels of lactate dehydrogenase activity. These indicated that hypoxic branched-chain amino acid synthesis is a unique alternative mechanism that functions in the absence of glucose-to-ethanol/lactate fermentation and oxygen respiration.

Protective effect of resveratrol against naphthalene-induced oxidative stress in mice

Objective This investigation confirms the role of free radicals in naphthalene-induced toxicity and elucidates the mechanism of resveratrol (RVT). Methods Both male and female BALB-c mice were administered with naphthalene (100 mg/kg, i.p.) for 30 days, either along with saline or along with RVT (10 mg/kg, orally). At the end of the experiment, following treatment and sacrifice of animals by decapitation, lung, liver and kidney tissue samples were taken for histological examination or determination of malondialdehyde (MDA), glutathione (GSH), myeloperoxidase (MPO) activity and collagen contents. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN) and creatinine levels and lactate dehydrogenase (LDH) activity were measured in the serum samples, while TNF- α, IL- β, IL-6 and total antioxidant capacity (AOC) were assayed in plasma samples. Results Naphthalene administration caused a significant decrease in tissue GSH and plasma AOC, which was accompanied with significant increases in tissue MDA and collagen levels and MPO activity. Moreover, the pro-inflammatory mediators (TNF- α, IL- β, IL-6), LDH activity, AST, ALT, creatinine and BUN levels were significantly increased in the naphthalene group. On the other hand, RVT treatment reversed all these biochemical indices as well as histopathological alterations induced by naphthalene. Conclusions Oxidative mechanisms play an important role in naphthalene-induced tissue damage, and RVT, by inhibiting neutrophil infiltration, balancing oxidant–antioxidant status, and regulating the generation of inflammatory mediators, ameliorates oxidative organ injury due to naphthalene toxicity.

Індукція апоптозу та некрозу лейкемічних клітин очищеними препаратами IgG сироватки крові мишей, яким тривалий час згодовували мозок великої рогатої худоби

IgG preparations of mice under study were tested for their ability to induce death of cells of L1210 line of murine leukemia. The highest level of cytotoxic activity was found at affecting cells with IgG of mice that were additionally fed with cattle brain. It was shown that the test cells were dying by both apoptosis (typical signs are destruction of DNA, revealed by the method of DNA-comets, condensation and fragmentation of chromatin, discovered by fluorescent microscopy of cells, stained with Hoechst 33342) and necrosis. The latter was estimated taking into account the level of lactate dehydrogenase activity, which appeared in cultural medium of L1210 cells, and by light microscopy after cell staining according to Romanovsky-Gimza.

Melatonin protects against endosulfan‐induced oxidative tissue damage in rats

Endosulfan is a chlorinated cyclodiene insecticide which induces oxidative stress. In this study, we investigated the possible protective effect of melatonin, an antioxidant agent, against endosulfan (Endo)-induced toxicity in rats. Wistar albino rats (n = 8) were administered endosulfan (22 mg/kg/day orally) followed by either saline (Endo group) or melatonin (10 mg/kg/day, Endo + Mel group) for 5 days. In other rats, saline (control group) or melatonin (10 mg/kg/day, Mel group) was injected for 5 days, following corn oil administration (vehicle of endosulfan). Measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content were performed in liver and kidney. Furthermore, aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), and creatinine levels, lactate dehydrogenase (LDH) activity were measured in the serum samples, while tumor necrosis factor-alpha (TNF-alpha), interleukin-beta (IL-beta) and total antioxidant capacity (AOC) were assayed in plasma samples. Endosulfan administration caused a significant decrease in tissue GSH and plasma AOC, which was accompanied with significant rises in tissue MDA and collagen levels and MPO activity. Moreover, the proinflammatory mediators (TNF-alpha and IL-beta), LDH activity, AST, ALT, creatinine and BUN levels were significantly elevated in the endosulfan-treated rats. On the other hand, melatonin treatment reversed all these biochemical alterations induced by endosulfan. Our results suggest that oxidative mechanisms play an important role in endosulfan-induced tissue damage and melatonin, by inhibiting neutrophil infiltration, balancing oxidant-antioxidant status and regulating the generation of inflammatory mediators, ameliorates oxidative organ injury as a result of endosulfan toxicity.

Pectolinarin and Pectolinarigenin of Cirsium setidens Prevent the Hepatic Injury in Rats Caused by D-Galactosamine via an Antioxidant Mechanism

To identify the hepatoprotective component from the leaves of Cirsium setidens (Compositae), the methanolic extract was divided into two fractions, chloroform and butanol fractions, and their hepatoprotective efficacy was evaluated in a rat model of hepatic injury caused by D-galactosamine (GalN). Hepatoprotective activity was measured by the activity of serum aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH). Glutathione metabolism was measured via biochemical parameters such as glutathione (GSH), glutathione reductase (GR), gamma-glutamylcysteine synthetase (GCS), glutathione S-transferase (GST), and superoxide dismutase (SOD) levels. We subjected the butanol fraction, which had higher activity, to column chromatography to yield pectolinarin, which was further hydrolyzed to yield pectolinarigenin. Administration (10, 20 mg/kg, p.o.) of the main flavonoid glycoside component, pectolinarin, and its aglycone, pectolinarigenin, for 2 weeks significantly decreased the activity levels of AST, ALT, ALP and LDH, indicating that the two compounds have hepatoprotective activity. Pectolinarin and pectolinarigenin also increased activity levels of GSH, GR, GCS, and GST, as well as SOD. The significant effect was only seen in SOD activity. This suggests that the two components exhibit hepatoprotective activity mainly via SOD antioxidant mechanism.

Efficacy and Toxicosis of VELCAP‐C Treatment of Lymphoma in Cats

Lymphoma is the most common malignancy affecting cats. A protocol employing vincristine, l-asparaginase, cyclophosphamide, doxorubicin, and prednisone (VELCAP-S) is effective and well tolerated in dogs with lymphoma. A 24-week variation of this protocol (VELCAP-C) was developed for treatment of cats. That VELCAP-C will result in survival times for cats with lymphoma that are similar to those obtained when cats are treated with a protocol that includes fewer chemotherapy agents. Sixty-one cats with lymphoma. Retrospective study. Outcomes evaluated were response to VELCAP-C therapy, toxicosis, and survival time. The effect of signalment, staging, CBC, and serum chemistry profile and dosage on these outcomes was examined. Six cats (10%) completed the protocol with a median survival of 1189 days. Forty-three percent (23 of 61) of the cats achieved complete response (CR) with a median survival time of 62 days. Cats that required a dose reduction of any drug during induction were more likely to achieve CR. Weight loss and hepatomegaly at diagnosis were negatively associated with response to treatment. Increased lactate dehydrogenase (LDH) serum activity at the time of initial treatment correlated with decreased survival times. This multi agent protocol did not provide improved survival over historical data using protocols with fewer agents. Serum LDH activity levels might provide useful prognostic information for cats with lymphoma.

Screening for periodontitis in pregnant women with salivary enzymes

To develop a test for the screening of pregnant women for periodontitis using saliva prior to a dental examination. A cross-sectional research design was employed. Whole unstimulated saliva was collected from 221 pregnant women prior to a dental examination at the Amagasaki Public Health Office and levels of activity of lactate dehydrogenase (LDH) and alkaline phosphatase (ALP), and of occult blood in the saliva were measured. The data were compared with Community Periodontal Index of Treatment Needs (CPITN) scores. The diagnostic performance of LDH, ALP, and occult blood was determined in terms of sensitivity, specificity, and the area under receiver operating characteristics (ROC) curves. The optimal combination of parameters for screening periodontitis was determined at maximum sensitivity and specificity. Periodontitis (CPITN 3, 4) in 19 women (8.6%) and gingivitis (CPITN 1, 2) in 129 women (58.4%) were observed. The activity levels of LDH and ALP were significantly higher in the pregnant women with periodontitis than those with gingivitis or a healthy periodontium. To distinguish between the pregnant women with periodontitis and the others, a cut-off value of 684 IU/L for LDH and of 75 IU/L for ALP were determined by a ROC analysis. The test combining LDH, ALP, and occult blood showed the highest diagnostic performance; with a sensitivity value of 0.90, specificity value of 0.62, positive predictive value of 0.18, and negative predictive value of 0.98. A test combining the parameters salivary LDH, ALP and occult blood is useful for screening pregnant women for periodontitis.

Using Lymphocyte and Plasma Hsp70 as Biomarkers for Assessing Coke Oven Exposure among Steel Workers

BackgroundHsp70, an early-response protein induced when organisms are confronted with simple or complicated environmental stresses, can act as either a cellular protector or a danger signal.ObjectivesThe goal of this study was to evaluate levels of lymphocyte and/or plasma Hsp70 as biomarkers for assessing exposure response to complex coke oven emissions (COEs).MethodsWe recruited 101 coke oven workers and determined levels of polycyclic aromatic hydrocarbon (PAH) exposure, urinary 1-hydroxypyrene (1-OHP), genotoxic damage by comet assay and micronuclei test, and other markers of damage, including plasma malondialdehyde (MDA) and lactate dehydrogenase (LDH). These were compared to levels of lymphocyte (intra-cellular) and plasma (extracellular) Hsp70 using Western blots and enzyme-linked immunosorbent assays (ELISA), respectively.ResultsWe observed a COEs-related dose-dependent increase in levels of DNA damage, micronuclei rate, MDA concentration, and LDH activity. Lymphocyte Hsp70 levels increased in the intermediate-exposure group (1.39 ± 0.88) but decreased in the high-exposure group (1.10 ± 0.55), compared with the low-exposure group. In contrast, plasma Hsp70 levels progressively increased as the dose of exposure increased. Negative correlations were seen between lymphocyte Hsp70 levels and olive tail moment and LDH activity in the intermediate- and high-exposure groups. However, we observed positive correlations between plasma Hsp70 levels and LDH activity in the low and intermediate groups.ConclusionsIn workers exposed to COEs, high lymphocyte Hsp70 levels may provide protection and high plasma Hsp70 levels may serve as a danger marker. Larger validation studies are needed to establish the utility of Hsp70 as a response marker.