Serum Lactate Dehydrogenase Activity Research Articles

Comparison of the effects of hesperidin over 30 and 60-day intervals on rainbow trout: a potential biostimulant to promote growth, immunological and antioxidant responses, and disease resistance

Abstract The current research evaluated the effects of dietary hesperidin (HSP) on growth parameters, digestive enzyme activities, innate immune markers, and antioxidant responses in rainbow trout, Oncorhynchus mykiss after the 30- and 60-day feeding trial. Then, specimens were subjected to Yersinia ruckeri infection for 14 days. For this, six hundred rainbow trout juveniles (initial weight; 25.49±0.40 g) were fed with different levels of HSP including 0 (HSP0; control), 50 (HSP50), 100 (HSP100), 150 (HSP150), and 200 (HSP200) mg/kg feed. After 60 days, dietary HSP100 supplementation significantly improved growth and feed efficiency indices. The optimal dose of HSP based on the regression test for WG and FCR detected 122 and 131mg/kg, respectively. At the end of the 30th day, dietary HSP150 supplementation markedly boosted serum lysozyme (LYZ), myeloperoxidase (MPO), complement component C3, and immunoglobulin (Ig) levels, as decreased malondialdehyde (MDA) content. In the same period, dietary administration of HSP at the different concentrations markedly increased complement component C4 (HSP150 and HSP200), superoxide dismutase (SOD), skin mucus alkaline phosphatase (ALP) (HSP100- HSP200), skin mucus LYZ and catalase (CAT) (HSP100 and HSP 150), and skin mucus Ig level (HSP50- HSP200). After 60 days, all dietary HSP supplementation significantly improved lipase, serum C3, glutathione peroxidase (GPX), and skin mucus ALP, LYZ, and Ig levels, but decreased MDA, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) values. After 60 days, dietary administration of HSP150 induced a significant discrepancy in the activity of serum LYZ, MPO, respiratory burst (RB), and lactate dehydrogenase (LDH) compared to the control group. In the same period, dietary HSP supplementation at different levels induced a remarkable increase in digestive protease activity (HSP100), serum ACH50 and CAT activities (HSP100 and HSP150), skin mucus peroxidase and serum SOD levels (HSP100-HSP200), and serum C4 value (HSP50, HSP150, and HSP200), but markedly decreased ALP activity (HSP150 and HSP200). In addition, dietary HSP supplementation, especially HSP150, markedly boosted disease resistance against Y. ruckeri infection. The current data demonstrated that the oral administration of 100 - 150 mg/kg HSP has a high potential to promote growth performance, disease resistance, and faster induction of immune and antioxidant responses.

H2S prevents the disruption of the blood-brain barrier in rats with prenatal hyperhomocysteinemia

Elevation of the homocysteine concentration in the plasma called hyperhomocysteinemia (hHCY) during pregnancy causes a number of pre- and postnatal developmental disorders. The aim of our study was to analyze the effects of H2S donors –NaHS and N-acetylcysteine (NAC) on blood-brain barrier (BBB) permeability in rats with prenatal hHCY. In rats with mild hHCY BBB permeability assessed by Evans Blue extravasation in brain increased markedly throughout life. Administration of NaHS or NAC during pregnancy attenuated hHCY-associated damage and increased endogenous concentrations of sulfides in brain tissues. Acute application of dl-homocysteine thiolactone induced BBB leakage, which was prevented by the NMDA receptor antagonist MK-801 or H2S donors. Rats with hHCY demonstrated high levels of NO metabolite – nitrites and proinflammatory cytokines (IL-1β, TNF-α, IL-6) in brain. Lactate dehydrogenase (LDH) activity in the serum was higher in rats with hHCY. Mitochondrial complex-I activity was lower in brain of hHCY rats. NaHS treatment during pregnancy restored levels of proinflammatory cytokines, nitrites and activity of the respiratory chain complex in brain as well as the LDH activity in serum. Our data suggest that H2S has neuroprotective effects against prenatal hHCY-associated BBB disturbance providing a potential strategy for the prevention of developmental impairments in newborns.

Benefits of Puerarin on Metabolic Syndrome and Its Associated Cardiovascular Diseases in Rats Fed a High-Fat/High-Sucrose Diet.

Metabolic syndrome (MetS) is a cluster of risk factors for cardiovascular diseases (CVDs) that has become a global public health problem. Puerarin (PUE), the principal active compound of Pueraria lobata, has the effects of regulating glucose and lipid metabolism and protecting against cardiovascular damage. This study aimed to investigate whether dietary supplementation with PUE could ameliorate MetS and its associated cardiovascular damage. Rats were randomly divided into three groups: the normal diet group (NC), the high-fat/high-sucrose diet group (HFHS), and the HFHS plus PUE diet group (HFHS-PUE). The results showed that PUE-supplemented rats exhibited enhanced glucose tolerance, improved lipid parameters, and reduced blood pressure compared to those on the HFHS diet alone. Additionally, PUE reversed the HFHS-induced elevations in the atherogenic index (AI) and the activities of serum lactate dehydrogenase (LDH) and creatine kinase (CK). Ultrasonic evaluations indicated that PUE significantly ameliorated cardiac dysfunction and arterial stiffness. Histopathological assessments further confirmed that PUE significantly mitigated cardiac remodeling, arterial remodeling, and neuronal damage in the brain. Moreover, PUE lowered systemic inflammatory indices including C-reactive protein (CRP), neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), and systemic immune-inflammation index (SII). In conclusion, dietary supplementation with PUE effectively moderated metabolic disorders, attenuated systemic inflammation, and minimized cardiovascular damage in rats with MetS induced by an HFHS diet. These results provide novel insights into the potential benefits of dietary PUE supplementation for the prevention and management of MetS and its related CVDs.

Exploration of Risk Factors of the Onset of Antibiotics-induced Acute Kidney Injury and Its Transfer to Chronic Kidney Disease Using the Medical Information Database

Drug-induced acute kidney injury (AKI) is a serious adverse drug reaction, which results in a significant decline in renal function and is known to progress to chronic kidney disease (CKD). Therefore, appropriate drug therapy is important to avoid the risk of drug-induced AKI and CKD, which are serious concerns in clinical practice. In this study, using the medical information database of Hamamatsu University Hospital, we investigated the risk factors that accelerate the onset of drug-induced AKI or its progression to CKD in patients who received aminoglycoside antibiotics (AGs) or glycopeptide antibiotics (GPs), which are strongly associated with drug-induced AKI and CKD. We performed logistic regression analysis using patients' background, laboratory test results, and concomitant drug use, among other such factors as explanatory variables and drug-induced AKI or CKD onset as objective variables to explore the risk factors for drug-induced AKI and CKD. Our results showed that co-administration of amphotericin B, piperacillin-tazobactam and other AGs and GPs, increased serum creatinine (Scr) and chloride concentrations, serum lactate dehydrogenase activity, and decreased serum albumin concentration were risk factors for drug-induced AKI onset. Moreover, a reduced blood urea nitrogen:Scr ratio at drug-induced AKI onset served as a risk factor for CKD. These results suggest that careful monitoring of the aforementioned factors is important to ensure appropriate usage of these drugs in patients treated with AGs and GPs.

Protective Effect of Dihydromyricetin Against ExerciseInduced Muscle Damage and Its Mechanism

Objective To investigate the protective effect of dihydromyricetin (DHM) against exercise-induced muscle damage (EIMD) in mice and its potential mechanism.Methods Adult male C57BL/6J mice were randomly divided into control group (CG), exercise group (EG), and exercise + 100 mg/kg weight ·d DHM (DHM) group. The intervention lasted for four weeks, during which the animals in the EG and DHM groups were subjected to exercise training for 1 h per day. The day after the training, a 90-min treadmill exercise (slope: 0 and speed: 18 m/min) was conducted in both EG and DHM groups. Samples of blood and gastrocnemius muscles were harvested from the three groups 24 h after the exercise, followed by the measurement of serum creatine kinase (CK) and lactate dehydrogenase (LDH) activities, total superoxide dismutase (T-SOD) activity, malondialdehyde (MDA), and skeletal muscle mitochondrial enzyme complex I and II activities. Histological changes in the skeletal muscle were observed by transmission electron microscopy, and the protein expressions of mitochondrial function-related pathways were detected by Western blotting.Results Skeletal muscle morphological changes and mitochondrial damage were alleviated in the DHM group compared to those in the EG. The activities of EIMD markers CK and LDH and the level of lipid peroxidation were notably repressed and the serum T-SOD activity was enhanced after DHM intervention. Western blotting demonstrated that the expressions of sirtuin type 3 (SIRT3), estrogen-related receptor alpha, and peroxisome proliferator-activated receptor-gamma coactivator-1 alpha in the skeletal muscle of mice increased after the DHM intervention.Conclusion DHM can relieve EIMD in mice, possibly by promoting the recovery of the mitochondrial structure and function in the skeletal muscle of mice after high-intensity exercise via the activation of the SIRT3 signaling pathway.

Biomarkers of oral subacute toxicity of deltamethrin in exposed male Albino rats.

Deltamethrin is one of the most effective pyrethroid compounds, widely employed in veterinary medicine, public health, and farming. Deltamethrin-triggered oxidative stress largely causes serious harm to an organism. Acute toxicity of this compound was extensively investigated, while less information is available on its oral sub-acute effects. This study assessed, in the male Albino rats, the effects of oral gavage of either 0.874mg/kg (0.01 LD50) or 8.740mg/kg (0.10 LD50) of deltamethrin for successive 14days to investigate its effects on biomarkers and to detect the tissue injury in rats following subacute deltamethrin treatment. It was found that levels of glutathione peroxidase, superoxide dismutase, and catalase in the brain, kidney, and liver, alkaline phosphatase (ALP), and uric acid in serum, hematocrit, mean corpuscular volume (MCV), white blood cells (WBC)s, eosinophils, and basophils were significantly reduced compared with untreated rats. However, when rats were treated with deltamethrin for successive 14days, alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) activities in serum and the levels of thiobarbituric acid reactive substances (TBARs) in brain, kidney, and liver, red blood cell distribution width (RDW-CV), total protein, monocytes, and basophils and the ratios of neutrophils to lymphocytes, an aggregated marker of systemic inflammation and systemic immune inflammation indexes, significantly increased compared with the control group. Histologic lesions were observed in the liver, kidney, brain, testis, and epidemies in rats exposed to subacute deltamethrin for 14days, and most tissues of rats treated with 0.10 LD50 of deltamethrin were more affected than those treated with 0.01 LD50. These findings strongly suggest that subacute exposure to deltamethrin caused significant systemic toxicity through oxidative stress resulting in biochemical and histological changes in the studied tissues. These findings highlight the potential harmful effects of deltamethrin and emphasize the importance of understanding the subacute effects of this compound, particularly in the context of veterinary medicine, public health, and farming.

Gentiopicroside ameliorates CCl4-induced liver injury in mice by regulating the PPAR-γ/Nrf2 and NF-κB/IκB signaling pathways.

This study explored the mechanisms by which gentiopicroside protects against carbon tetrachloride (CCl4)-induced liver injury. Male mice were randomly assigned to the control; CCl4; bifendate 100 mg/kg; or gentiopicroside 25, 50, or 100 mg/kg groups. Both vehicle and drugs were administered intragastrically for 7 days. Mice were administered CCl4 intraperitoneally 1 hour after the last drug dose. After 24 hours, we collected blood and liver samples for testing. Gentiopicroside significantly reduced serum alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase activities with corresponding reductions in hepatocyte denaturation and necrosis. Gentiopicroside enhanced superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and glutathione levels and reduced heme oxygenase 1 (HO-1) activity and malondialdehyde levels in the liver, and these effects were attributed to peroxisome proliferator-activated receptor (PPAR)-γ/nuclear factor erythroid 2-related factor 2 (Nrf2) activation. Meanwhile, gentiopicroside significantly downregulated HO-1 and upregulated SOD and GSH-Px at the mRNA level in the liver. Furthermore, gentiopicroside significantly suppressed serum tumor necrosis factor-α and interleukin-1β secretion, which was associated with the inhibition of nuclear factor-kappa B (NF-κB)/inhibitor of NF-κB (IκB). Gentiopicroside ameliorated CCl4-induced liver injury in mice via the PPAR-γ/Nrf2 and NF-κB/IκB pathways.

Inflammation alters iron distribution in bone and spleen in mice.

Anemia of inflammation (or inflammation-associated anemia) decreases the quality of life in billions of patients suffering from various inflammatory diseases, such as infection, autoimmune diseases, and cancer, associated with a prolonged state of immune activation. While proper utilization of iron, a nutrient metal essential for erythropoiesis, is important for the prevention of anemia, the alteration of body iron homeostasis upon inflammation, which can contribute to the development of anemia, is not completely understood. Thus, we sought to examine temporal and spatial changes in the distribution of iron and iron-associated molecules during inflammation in mice. To induce inflammation, C57BL/6J mice were injected with turpentine oil weekly for 3 weeks, which resulted in anemia, decreased protein expression of ferroportin, a cellular iron exporter, in the spleen, duodenum, and liver, and increased iron stores in the duodenum and spleen. Tracer kinetic studies after oral administration of 59Fe revealed that more iron was found in the spleen and less in the femur bone in turpentine oil-injected mice compared to the saline-injected mice, indicating tissue-specific abnormalities in iron distribution during inflammation. However, there was no difference in the utilization of iron for red blood cell production after turpentine oil injection; instead, serum hemopexin level and lactate dehydrogenase activity were increased, suggesting increased red blood cell destruction upon inflammation. Our findings provide an improved understanding of temporal and spatial changes in the distribution and utilization of iron during inflammation.

Effects of Ocimum basilicum essential oil and ginger extract on serum biochemistry, oxidative stress and gill tissue damage of pearl gentian grouper during simulated live transport.

This study explored the effects of the essential oil of Ocimum basilicum (EOOB) and ginger extract (GE) during the transportation of pearl gentian grouper from water quality, serum biochemistry, oxidative stress, meat flavor, and gill tissue morphology. Fish (450 ± 50g) were allocated to the following 5 treatments: control group (fish transported in water only), 5mg/LEOOB, 10mg/LEOOB, 3mg/LGE, and 6mg/LGE and transported in insulation boxes (66 × 51 × 37.8cm) for 72h. Samples were taken at 0, 12, 36, 60, and 72h immediately after transport. It was found that 10mg/LEOOB and 6mg/LGE could reduce the levels of total ammonia nitrogen (TAN), dissolved oxygen (DO), water pH, serum glucose (GLU), cortisol (COR), liver superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), and glutathione peroxidase (GPX), increase the activities of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH), as well as significantly increase the total free amino acid (TFAA) content in muscle compared to the control group (P < 0.05). In addition, by observing the microstructure of gill tissue, it was found that compared with untreated grouper, the morphological damage of gill tissue in EOOB and GE treatment was alleviated. These results indicated that adding appropriate amounts of EOOB and GE to transport water could improve the water quality, relieve stress, and lower energy metabolism of grouper during transport. The results of this research will help to improve the survival rate of grouper after transportation and decrease economic losses to fishery.

Photometric flow system for the determination of serum lactate dehydrogenase activity

The routine method for LDH (Lactate dehydrogenase) activity determination is to monitor the increase of NADH concentration at 340 nm. There are some inconvenience in taking measurements in the near-UV region, especially in the case of serum samples analysis. In this work, two modifications of the routine LDH activity assay based on the use of reducing properties of NADH have been compared. Both methods involved the reduction of compounds that can be easily determined by well-known methods, ferric ion (with ferrozine) and nitrotetrazolium blue (NBT). A fully-mechanized Multicommutated Flow Analysis-Paired Emitter Detector Diode (MCFA-PEDD) system based on solenoid devices was developed and applied for both methods. The linear ranges obtained for Fe-ferrozine and NBT methods are 6.0–200.0 U L−1 and 10.0–250.0 U L−1 with estimated detection limits at 0.2 U L−1 and 4.5 U L−1, respectively. The low LOQ values enabled 10-fold sample dilutions, which is advantageous for samples with limited available volume. The Fe-ferrozine method is more selective for LDH activity in the presence of glucose, ascorbic acid, albumin, bilirubin, copper and calcium ions than NBT method. To confirm the analytical usefulness of the proposed flow system, the analysis of real human serum samples was carried out. The statistic tests showed satisfactory correlation between the results obtained for both developed methods and those received using the reference method.

A retrospect study based on real-world data to observe metabolic function in cancer patients using albumin-bound paclitaxel

There is substantial evidence that albumin-bound paclitaxel (nab-paclitaxel) is effective and safe for the treatment of breast, lung and pancreatic cancers. However, it can still cause adverse effects by affecting cardiac enzymes, hepatic enzyme metabolism and blood routine related indicators, which affects the use of chemotherapy for a full course of treatment. However, there are no relevant clinical studies to systematically observe the effects and dynamics of albumin-bound paclitaxel on cardiac enzymes, liver enzyme metabolism, and routine blood-related indices. The purpose of our study was to determine the levels of serum creatinine (Cre), aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatine kinase (CK), creatine kinase isoenzyme (CK-MB), white blood cells (WBC) and hemoglobin (HGB) in cancer patients treated with albumin-conjugated paclitaxel. This study retrospectively analyzed 113 patients with cancer. Patients who had received two cycles of nab-paclitaxel 260 mg/m2 (administered intravenously on days 1, 8, and 15 of each 28-day cycle) were selected. Serum Cre, AST, ALT, LDH, CK, and CK-MB activities, WBC counts, and HGB levels were measured before and after treatment with two cycles. Fourteen cancer types were analyzed. The distribution of cancer types in patients was mainly concentrated in lung, ovarian, and breast cancer. Nab-paclitaxel treatment markedly decreased Cre, AST, LDH, and CK activities in the serum and WBC counts and HGB levels, respectively. Serum Cre and CK activities and HGB levels were remarkably downregulated at baseline compared to healthy controls. Patients receiving nab-paclitaxel treatment cause metabolic disorders in tumor patients by reducing the decrease of Cre, AST, LDH, CK, CK-MB, WBC and HGB indexes, thus inducing the occurrence of cardiovascular events, hepatotoxic events and fatigue and other symptoms. Therefore, for tumor patients, although receiving nab-paclitaxel improves the anti-tumor effect, it is still necessary to closely monitor the changes of related enzymatic and routine blood indicators, so as to detect and intervene at an early stage.

Rutin and Hesperidin Revoke the Hepatotoxicity Induced by Paclitaxel in Male Wistar Rats via Their Antioxidant, Anti-Inflammatory, and Antiapoptotic Activities.

Paclitaxel, one of the most effective chemotherapeutic drugs, is used to treat various cancers but it is exceedingly toxic when used long-term and can harm the liver. This study aimed to see if rutin, hesperidin, and their combination could protect male Wistar rats against paclitaxel (Taxol)-induced hepatotoxicity. Adult male Wistar rats were subdivided into 5 groups (each of six rats). The normal group was orally given the equivalent volume of vehicles for 6 weeks. The paclitaxel-administered control group received intraperitoneal injection of paclitaxel at a dose of 2 mg/Kg body weight twice a week for 6 weeks. Treated paclitaxel-administered groups were given paclitaxel similar to the paclitaxel-administered control group together with oral supplementation of rutin, hesperidin, and their combination at a dose of 10 mg/Kg body weight every other day for 6 weeks. The treatment of paclitaxel-administered rats with rutin and hesperidin significantly reduced paclitaxel-induced increases in serum alanine transaminase, aspartate transaminase, lactate dehydrogenase, alkaline phosphatase, and gamma-glutamyl transferase activities as well as total bilirubin level and liver lipid peroxidation. However, the levels of serum albumin, liver glutathione content, and the activities of liver superoxide dismutase and glutathione peroxidase increased. Furthermore, paclitaxel-induced harmful hepatic histological changes (central vein and portal area blood vessel congestion, fatty changes, and moderate necrotic changes with focal nuclear pyknosis, focal mononuclear infiltration, and Kupffer cell proliferation) were remarkably enhanced by rutin and hesperidin treatments. Moreover, the elevated hepatic proapoptotic mediator (caspase-3) and pro-inflammatory cytokine (tumor necrosis factor-α) expressions were decreased by the three treatments in paclitaxel-administered rats. The cotreatment with rutin and hesperidin was the most effective in restoring the majority of liver function and histological integrity. Therefore, rutin, hesperidin, and their combination may exert hepatic protective effects in paclitaxel-administered rats by improving antioxidant defenses and inhibiting inflammation and apoptosis.

The bio-derived material acacetin ameliorated hyperlipidemia and intestinal barrier damage in mice by modulating gut microbiota

The increasing incidence of hyperlipidemia has been linked to disruptions in gut flora. The bio-derived material, acacetin, is a naturally flavonoid compound extracted from various plants that has been shown to protect the liver and lowers blood lipid levels, its potential to mitigate gut barrier damage caused by a high-fat diet (HFD) has not been fully explored. This work aimed to investigate the effects of acacetin on HFD-induced intestinal barrier disruption and its potential interaction with gut microbiota regulation. Forty-eight female ICR mice were divided into three groups: control group (standard diet containing 6% daily energy from fat), HFD group (45% of daily energy from fat), and the acacetin (AC) group (HFD with acacetin 30 mg/kg body weight). The test period lasted for eight weeks. In addition to lipid metabolism parameters, serum lactate dehydrogenase (LDH) activity, diamine oxidase (DAO) activity, and lipid metabolism, we used the real-time fluorescence quantitative method to measure the expression of zonula occludens 1 (ZO-1) and occludin genes. The microorganisms were analyzed by 16 s RNA and functional gene prediction analysis. The results indicated that acacetin treatment could alter serum biochemical parameters and reduce body weight, liver weight gain, and abdominal fat accumulation. Furthermore, acacetin increased the expression levels of ZO-1 and occludin in HFD mice. In addition, acacetin altered the structure, diversity, and function of intestinal flora, characterized by the restoration of the Firmicutes/Bacteroidetes ratio. Additionally, the species abundance were significant correlation with lipid factors, DAO, and LDH. Alistipes and Acetatifactor were the prevalent genus in the AC group. Acacetin downregulated HFD-induced Facultative_anaerobic phenotypes related to Clostridium according to the BugBase analysis. The KEGG study revealed that acacetin altered the functional composition of microorganisms, as evidenced primarily by variations in the abundance of metabolic pathways involved in lipid metabolism and intestinal epithelial injury. The COG category showed acacetin increased the abundance of Cytoskeleton associated with the intestinal barrier. Overall, acacetin ameliorated HFD-induced hyperlipidemia and intestinal barrier damage in mice by modulating intestinal bacteria, exhibited a good clinical application prospect.

Investigation of the efficacy of diosmin against organ damage caused by bendiocarb in male Wistar albino rats.

Bendiocarb is a carbamate insecticide, which is used more in indoor areas, especially against scorpions, spiders, flies, mosquitoes and cockroaches. Diosmin is an antioxidant flavonoid found mostly in citrus fruits. In this study, the efficacy of diosmin against the adverse effects of bendiocarb was investigated in rats. For this purpose, 60, 2-3month-old male Wistar albino rats, weighing 150-200g, were used. The animals were assigned to six groups, one of which was maintained for control purposes and five of which were trial groups. The control rats received only corn oil, which was used as a vehicle for diosmin administration in the trial groups. Groups 2, 3, 4, 5 and 6 were administered with 10mg/kg.bw bendiocarb, 10mg/kg.bw diosmin, 20mg/kg.bw diosmin, 2mg/kg.bw bendiocarb plus 10mg/kg.bw diosmin, and 2mg/kg.bw bendiocarb plus 20mg/kg.bw diosmin, respectively, using an oral catheter, for 28days. At the end of the study period, blood and organ (liver, kidneys, brain, testes, heart and lungs) samples were collected. Body weight and organ weights were determined. Compared to the control group, in the group given bendiocarb alone, firstly, body weight and liver, lung and testicular weights decreased. Secondly, tissue/plasma malondialdehyde (MDA) and nitric oxide (NO) levels increased, and glutathione (GSH) levels and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) (except for lung tissue), glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G6PD) activities decreased in alltissues and erythrocytes. Thirdly, catalase (CAT) activity decreased in erythrocytes and the kidney, brain, heart and lung tissues and increased in the liver and testes. Fourthly, while GST activity decreased in the kidneys, testes, lung and erythrocytes, an increase was observed in the liver and heart tissues. Fifthly, while serum triglyceride levels and lactate dehydrogenase (LDH), alkaline phosphatase (ALP) and pseudo-cholinesterase (PchE) activities decreased, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities and blood urea nitrogen (BUN), creatinine and uric acid levels increased. Lastly, liver caspase 3, caspase 9 and p53 expression levels significantly increased. When compared to the control group, the groups treated with diosmin alone showed no significant difference for the parameters investigated. On the other hand, it was observed that the values of the groups treated with a combination of bendiocarb and diosmin were closer to the values of the control group. In conclusion, while exposure to bendiocarb at a dose of 2mg/kg.bw for 28days caused oxidative stress/organ damage, diosmin administration at doses of 10 and 20mg/kg.bw reduced this damage. This demonstrated that diosmin has pharmaceutical benefits, when used for supportive treatment as well as radical treatment, against the potential adverse effects of bendiocarb.

The protective effects of baicalin and chrysin against emamectin benzoate-induced toxicity in Wistar albino rats.

The aim of this study was to investigate the effects of baicalin, chrysin and their combinations against emamectin benzoate-induced toxicity in rats. For this purpose, sixty four rats were divided into evenly8 groups with 6-8-week-old male Wistar albino rats, weighing 180-250g, in each group. While the first group was kept as a control (corn oil), the remaining 7 groups were administered with emamectin benzoate (10mg/kg bw), baicalin (50mg/kg bw) and chrysin (50mg/kg bw) alone or together for 28days. Oxidative stress parameters, serum biochemical parameters and blood/tissue (liver, kidney, brain, testis and heart) and tissue histopathology were investigated. Compared to the control group, the emamectin benzoate-intoxicated rats had significantly higher tissue/plasma concentrations of nitric oxide(NO) and malondialdehyde(MDA), as well as lower tissue glutathione(GSH) concentrations and antioxidant enzyme activity (glutathione peroxidase/GSH-Px, glutathione reductase/GR, glutathione-S-transferase/GST, superoxide dismutase/SOD, catalase/CAT). Biochemical analysis showed that emamectin benzoate administration significantly increased serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) activities, as well as triglyceride, cholesterol, creatinine, uric acid and urea levels, and decreased serum total protein and albumin levels. The histopathological examination of the liver, kidney, brain, heart and testis tissues of the emamectin benzoate-intoxicated rats demonstrated necrotic changes. Baicalin and/or chrysin reversed the biochemical and histopathological alterations induced by emamectin benzoate on these tested organs. Therefore, baicalin and chrysin (alone or in combination) could offer protection against emamectin benzoate-induced toxicity.

Investigation of the biological activity of the water-soluble C&lt;sub&gt;60&lt;/sub&gt;/poly-&lt;i&gt;N&lt;/i&gt;-vinylpyrrolidone complex

Objectives. The study aimed to investigate the biological activity of the C60/poly-N-vinylpyrrolidone (C60/PVP) complex representing a water-soluble fullerene derivative. In vitro and in vivo techniques were used to analyze the effect of the C60/PVP complex on the activity of lactate dehydrogenase (LDH) and evaluate changes in the biochemical parameters of blood serum when per os administered to mice.Methods. In order to determine the activity of a commercial LDH preparation and study the kinetics of this process, the standard Warburg photometric method was used. To assess the effect of polyvinylpyrrolidone (PVP) and the C60/PVP complex on some biochemical parameters in vivo, a study was conducted on two-month-old male white mongrel mice weighing 20 ± 3 g. Determination of biochemical parameters of blood serum was carried out using a semi-automatic biochemical analyzer according to standard methods.Results. The effect of the C60/PVP complex on LDH activity was studied along with changes in the biochemical parameters of mouse blood serum characterizing carbohydrate metabolism. As well as increasing the glucose and pyruvic acid content, the C60/PVP complex was found to reduce lactate content and LDH activity in blood serum along with in vitro LDH activity according to the type of mixed inhibition.Conclusions. The C60/PVP complex and PVP were shown to exhibit biological activity in vitro and in vivo. The C60/PVP complex, representing a mixed-type LDH inhibitor, was shown to inhibit LDH activity, as well as contributing to a decrease in lactate concentration and an increase in the concentration of pyruvic acid and glucose in blood serum when administered per os to mice. The inhibitory effect of PVP on LDH activity was revealed in both in vivo and in vitro investigations. In vivo, PVP contributes to a decrease in the concentration of lactate in the blood. The less pronounced effect of the C60/PVP complex as compared to PVP alone may be due to the fact that C60 molecules are “hidden” in cavities formed in PVP molecules.

Effects of Psidium guajava and Ribes americanum Aqueous Extracts and Dietary Modification on some Markers of Renal, Cardiac Dysfunction in Rats

The effect of aqueous extract of P. guajava and R. americanum and dietary modification interactions on serum renal function markers levels (urea, creatinine) cardiac function markers (lactate dehydrogenase, creatinine kinase), serum ions (calcium, sodium, and potassium ions) were investigated in rats. Fully grown Wister strain rats were exposed to high fat and salted diet formulation and treated with the aqueous extract for a period of 6 weeks. The diets were formulated by adding 25% animal fat and 5% palm oil to standard feeds (Vital feeds, Bukuru Jos, Plateau. Significant decrease in serum urea, creatinine, and lactate dehydrogenase and creatine kinase activities in the group treated with P. guajava and R. americanum aqueous extract compared to the high fat-salted water group. There was no significant difference in plasma urea and Creatinine, LDH and CK levels between the standard feeds and standard feed plus salted water group. Significant increase in the plasma Creatinine and lactate dehydrogenase levels (at p&lt;0.05) of the high-fat plus salted water group when compared with the high fat group. Significant (at p&lt;0.05) increase in serum sodium of the group exposed to salted water when compared with the non-salted water group. There was a significant (p&lt;0.05) decrease in serum sodium levels of extract administered groups compared to the high fat-salted water and standard feed salted water groups. There was also a significant increase, at p&lt;0.05, in serum potassium and calcium of the extracts administered group when compared with the standard feed salted water, high fat and high fat salted water groups. The study showed that the combined effects of high fat and high salt increased serum sodium and decreased serum potassium and calcium. Administration of the aqueous extract administration reversed by the effects

17beta-estradiol alleviates contusion-induced skeletal muscle injury by decreasing oxidative stress via SIRT1/PGC-1α/Nrf2 pathway

PurposeThis study aimed to investigate the role of 17β-estradiol (E2) in the repair of contusion-induced myoinjury in mice and to identify the underlying molecular mechanisms. MethodsIn vivo, contusion protocol was performed for preparing mice myoinjury model, and Injection (i.p.) of 17β-estradiol (E2) or estrogen receptor antagonist ICI 182,780, or ovariectomy (OVX), was used to alter estrogen level of animal models. In vitro, C2C12 myoblasts were treated with H2O2 (oxidative stress inducer), SIRT1 inhibitor EX527, or aromatase inhibitor anastrozole. Serum E2 level was assessed by enzyme-linked immunosorbent assay (ELISA). Muscle damage repair was evaluated by H&E staining and the activities of serum creatine kinase (CK) and lactate dehydrogenase (LDH). The oxidative stress was estimated by the levels of catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA). Western blot was performed to measure the protein expressions of SIRT1, PGC-1α, Nrf2, and HO-1. ResultsWe observed the elevated serum E2 levels and the upregulated oxidative stress in damaged muscle in female mice after contusion-induction. The E2 administration in vivo alleviated contusion-induced myoinjury in OVX mice by reducing CK and LDH activities, suppressing oxidative stress, and enhancing the expression levels of SIRT1, PGC-1α, Nrf2, and HO-1. These effects were inhibited by treatment with an ERα/β antagonist. Moreover, EX527 or anastrozole treatment exacerbated H2O2-induced growth inhibition and oxidative stress, and expression downregulation of SIRT1, PGC-1α, Nrf2, and HO-1 in C2C12 cells in vitro. ConclusionOur results suggest that E2 is a positive intervention factor for muscle repair followed contusion-induced myoinjury, through its effects on suppressing oxidative stress via activating the SIRT1/PGC-1α/Nrf2 pathway.

Alleviation of negative effect of heat stress through supplementations of cinnamon (Cinnamomum zeylanicum) and turmeric (Curcuma longa L) powders in diets of broiler chickens

This study was designed to assess the effect of cinnamon powder (CNP) and turmeric powder (TP) on growth performance, antioxidant status, liver function, meat quality and lactate dehydrogenase activity of broiler chickens under heat stress conditions. A total of 200, one day old as-hatched broiler chickens (ROSS 308) were randomly allotted into five treatments with four replicates (n = 10). Treatment groups were control (C): fed basal diet; T1: 0.5% CNP; T2: 1.0% CNP; T3: 0.5% TP and T4: 1.0% TP. Results indicated that body weight gain, feed intake and feed conversion ratio were improved significantly (p < 0.05) in treatments fed CNP and TP. Serum malondialdehyde and lactate dehydrogenase activity were decreased (p < 0.05) while blood superoxide dismutase, catalase and glutathione peroxidase activity were increased (p < 0.05) in treatments fed CNP and TP. Addition of CNP and TP decreased (p < 0.05) serum aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase activity. Treatments fed CNP and TP resulted increased (p < 0.05) breast and thigh meat monounsaturated fatty acid, polyunsaturated fatty acid, linoleic acid, oleic acid and water holding capacity while decreased (p < 0.05) saturated fatty acid and cook loss. In conclusion CNP and TP possess advantageous effect on growth performance, antioxidant status, liver function, meat quality and lactate dehydrogenase activity.

Ent-kaurenoic acid-enriched Mikania glomerata leaves-complexed β-cyclodextrin: Pharmaceutical development and in vivo antitumor activity in a sarcoma 180 mouse model

The extract obtained from Mikania glomerata leaves rich in ent-kaurenoic acid (ERKA) shows cytotoxic activity in vitro, but its hydrophobic nature and thermosensitivity are issues to be solved prior to in vivo antitumor studies. The purpose of this study was to investigate the antitumor activity of inclusion complexes formed between ERKA and β-cyclodextrin (ERKA:β-CD) in rodents. ERKA:β-CD complexes obtained by malaxation (MX) and co-evaporation (CE) methods were firstly characterized regarding their physical properties, encapsulation efficiency, and cytotoxicity againts L929 cells. The antitumor activity study was then performed in mice with sarcoma 180 treated with saline, 5-fluouracil (5FU) and ERKA:β-CD at 30, 100 and 300 µg/kg. The weight, volume, percentage of inhibition growth, gross and pathological features and positivity for TUNEL, ki67, NFκB and NRF2 in the tumors were assessed. Serum lactate-dehydrogenase activity (LDH), white blood cells count (WBC) and both gross and pathological features of the liver, kidneys and spleen were also evaluated. The formation of the inclusion complexes was confirmed by thermal analysis and FTIR, and they were non-toxic for L929 cells. The MX provided a better complexation efficiency. ERKA:β-CD300 promoted significant tumor growth inhibition, and attenuated the tumor mitotic activity and necrosis content, comparable to 5-fluorouracil. ERKA:β-CD300 also increased TUNEL-detected cell death, reduced Ki67 and NF-kB immunoexpression, and partially inhibited the serum LDH activity. No side effect was observed in ERKA:β-CD300-treated animals. The ERKA:β-CD inclusion complexes at 300 µg/kg displays antitumour activity in mice with low systemic toxicity, likely due to inhibition on the NF-kB signaling pathway and LDH activity.