Serum myeloperoxidase, paraoxonase, and plasma asprosin concentrations in patients with acute myocardial infarction.

Introduction: The objective of this study was to evaluate the usefulness of the serum biomarkers myeloperoxidase (MPO), paraoxonase (PON), and plasma asprosin in acute myocardial infarction (AMI) diagnosis and assess their compatibility with routinely screened cardiac biomarkers. Methods: This study was conducted using a prospective cross-sectional design and included 90 patients, consisting of 60 patients diagnosed with AMI (30 with ST-segment elevation and 30 with non-ST-segment elevation on ECG) and 30 controls (without a diagnosis of AMI). Changes in the levels of cardiac biomarkers (Hs-cTnI, CK, CK-MB), lipid profile (TC, TG, LDL, HDL), MPO, PON, asprosin, and routine biochemical parameters of patients were evaluated. Furthermore, receiver operating characteristic curve analysis revealed the diagnostic value of Hs-cTnI, MPO, PON, and asprosin in predicting AMI. Binary logistic regression analysis of cardiac marker concentrations was used to predict the presence of AMI. In contrast, multinomial logistic regression analysis was conducted to predict the type of AMI and the control group. Results: The median levels of MPO and plasma asprosin were found to be higher in the patient group (3.22 [interquartile range {IQR}: 2.4-4.4] ng/ml and 10.84 [IQR: 8.8-17.8] ng/ml, respectively) than in the control group (2.49 [IQR: 1.9-2.9] ng/ml and 4.82 [IQR: 4.6-8.0] ng/ml, respectively) (p = 0.001 and p < 0.001, respectively). The median levels of PON were 8.94 (IQR: 7.6-10.4) ng/ml in the patient group and 10.44 (IQR: 9.1-20.0) ng/ml in the control group (p < 0.001). In the binary logistic regression model, compared with the control group, a 1 ng/ml increase in MPO level increased the odds of having AMI by 3.61 (p = 0.041, 95% CI: 1.055-12.397), whereas a 1 ng/ml increase in asprosin level increased the odds of having AMI by 2.33 (p < 0.001, 95% CI: 1.479-3.683). In the multinominal logistic regression model, compared with the control group, a 1 ng/ml increase in the MPO level increased the odds of having NSTEMI by 4.14 (p = 0.025, 95% CI: 1.195-14.350), whereas a 1 ng/ml increase in asprosin concentrations increased the odds of having NSTEMI by 2.35 (p < 0.001, 95% CI: 1.494-3.721). Conclusion: Herein, MPO and asprosin concentrations increased with Hs-cTnI, and a decrease in PON concentration indicated that oxidant-antioxidant parameters and adipokines were related to AMI pathogenesis.

Protective effect of astaxanthin on experimental ovarian damage in rats.

This study aimed to investigate the protective effect of astaxanthin (AS) on 3-nitropropionic acid (3-NPA) induced experimental ovarian damage in rats. Thirty two female Wistar rats were divided into four equal groups of eight each: control group (C); phosphate-buffered saline, AS group; AS (80 mg/kg) for 14 days, 3-NPA group; 3-NPA (6.25 mg/kg) twice a day for 7 days, 3-NPA + AS group; administered AS (80 mg/kg) for 14 days and 3-NPA (6.25 mg/kg) for 7 days. All injections were administered intraperitoneally. Rats were fed ad libitum with standard rat chow and tap water. Plasma and ovarian tissue total antioxidant capacity (TAC), total oxidant capacity (TOC) and oxidative stress index (OSI) levels, whole blood reduced glutathione (GSH), plasma paraoxonase 1 (PON1) activity, lipid profile, malondialdehyde (MDA), nitric oxide (NO), total sialic acid (TSA) and total thiol (TT) concentrations were analysed spectrophotometrically. Also, ovarian tissue histopathology was performed. We observed 3-NPA-induced histopathological ovarian damage significantly decreased the TAC (p < 0.001), GSH (p < 0.001), high-density lipoprotein (p < 0.01) levels and PON1 activity (p < 0.01), and significantly increased TOC, OSI (p < 0.001), MDA, NO, TSA, cholesterol, low-density lipoprotein (p < 0.01) and triglyceride (p < 0.05) levels. In conclusion, cotreatment with AS restored the negative effect of 3-NPA on all biochemical parameters cited above and improved the histopathological ovarian damage. Ovarian toxicity induced by 3-NPA might be due to oxidative damage. The improvement of AS seems to be related to its antioxidant properties.

Chlorpyrifos-induced parkinsonian model in mice: Behavior, histopathology and biochemistry.

INTRODUCTION: The aim of this study was to investigate the protective effect of caffeic acid phenethyl ester (CAPE) on Paraoxonase (PON1) activity, and levels of lipid profile, total sialic acid (TSA), total antioxidant capacity (TAC) and total oxidant capacity (TOC) in the plasma and brain tissue of mice with chlorpyrifos-ethyl (CPF)-induced Parkinson. MATERIAL AND METHOD: In the study, 35 male Swiss albino mice were divided into 5 groups including equal number of mice as follows; intraperitoneal injection of saline for mice in control (C) group, subcutaneous injection of 80mg/kg CPF for CPF group, intraperitoneal injection of 10µmol/kg CAPE for CAPE group, subcutaneous injection of 80mg/kg CPF and intraperitoneal injection of 10µmol/kg CAPE for CPF+CAPE group and intraperitoneal injection of 10% ethanol diluted in physiological saline solution for 21days for ethanol (E) group. All the mice were fed with normal feed and tap water ad libitum. At the end of the study, PON1 activity, lipid profile (except for brain), and TSA, TAC and TOC levels in the plasma and brain tissue were analyzed. Tissue samples of brain substantia nigra were evaluated histopathologically. RESULTS: Levels of plasma TAC, high density lipoprotein (HDL) and PON1 activity were statistically lower in CPF group than the other groups (P<0.001). Also, levels of plasma TOC, TSA, total cholesterol, triglycerides, low density lipoprotein (LDL) and very low density lipoprotein (VLDL) were statistically higher in CPF group than the other groups(P<0.001). PON1 activity and level of TAC were significantly lower in brain tissue of CPF groups (P<0.001). In addition, TOC and TSA levels were significantly higher in brain tissue in CPF group (P<0.001). CONCLUSION: In conclusion, CAPE showed a protective effect on PON1 activity and levels of lipid profile, TSA, TAC and TOC in plasma and brain tissue and prevented the neurodegenerations in brain tissue in CPF-induced Parkinson's disease.

Oleuropein ameliorates arsenic induced oxidative stress in mice.

The objective of this study is to investigate the potential preventive effect of oleuropein in an experimental arsenic toxicity in mice. For this purpose, mice were exposed to 5mg/kg/day sodium arsenite (NaAsO2) in drinking water and treated with 30mg/kg/day oleuropein for 15 days. At the end of the experiment, animals were sacrificed and selected organs were processed for biochemical and histopahtological investigations. Blood, liver, kidney and brain malondialdehyde (MDA) and nitric oxide (NO) levels were determined by colorimetric methods. Protein carbonyl content is measured by a commercial kit. Liver morphology and immunoreactivity for inducible NOS (iNOS) and endothelial NOS (eNOS) was evaluated microscopically. Level of NO was determined to decrease in blood and tissues whereas MDA increased in arsenic given mice. Tissue protein carbonyl content also increased in this group. Immunoreactivity for iNOS and eNOS was noted to increase with arsenic treatment. Oleuropein treatment had significant effects in normalizing the MDA and NO levels as well as protein carbonyl content. Immunohistochemical staining also showed reduction of the expression of iNOS and eNOS in liver. The results indicate that oleuropein ameliorates oxidative tissue damage by scavenging free radicals.

Investigation of protective effect of L-carnitine on L-asparaginase-induced acute pancreatic injury in male Balb/c mice.

INTRODUCTION: The present analysis deals with the biochemical and histopathological effects of L-carnitine in mice with L-asparaginase (ASNase)-induced experimental acute pancreatic injury (API). METHODS: A total of 32 male Balb/c mice were divided into four groups as follows. Group I (control) was injected with single saline via the intraperitoneal route. Group II received 500 mg/kg of L-carnitine daily with the injected volume of 62.5-75 µl for 25-30 g mice using a Hamilton microinjector applied for 5 days. Group III received a single 10,000 IU Escherichia coli ASNase/kg body weight dose of ASNase at a dose of 500 mg/kg. Group IV received 500 mg/kg of L-carnitine daily and a single dose of 500 mg/kg of ASNase and were decapitated on the fifth day following the injection. Blood and pancreatic tissue samples were obtained for evaluation of histopathological structure and levels of malondialdehyde (MDA), reduced glutathione (GSH), total sialic acid (TSA), glucose, amylase and triglyceride. RESULTS: In group III, compared to group IV and group I it was determined that levels of GSH and amylase were significantly lower while levels of MDA, TSA, glucose and triglyceride were higher. Levels of GSH, MDA, TSA, glucose, triglyceride and amylase, especially in group IV, approached that of group I. As a result, L-carnitine for ASNase-induced API mice may be protective against pancreatic tissue degeneration and oxidative stress or lipid peroxidation.

Protective effect of omega-3 fatty acid against mercury chloride intoxication in mice.

The aim of this study was to investigate the protective effect of omega-3 fatty acid in HgCI2 toxicity in mice. Levels of malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (NO) and total sialic acid (TSA), and histopathological changes in selected organs were evaluated. Twenty-eight mice were equally divided into 4 groups, namely Groups I-IV. Group I animals received intraperitoneal (ip) injection of physiological saline solution; Group II animals received ip injection of 0.4mg/kg/day HgCI2; Group III animals received ip injection of 0.4mg/kg/day HgCI2 in addition to subcutaneous (sc) injection of 0.5g/kg/day omega-3 fatty acid; and Group IV animals received sc injection of 0.5g/kg/day omega-3 fatty acid. All treatments lasted 7 days. The levels of MDA, NO and TSA were significantly higher in Group II and lower in Groups III and IV as compared to the Group I. GSH level was the highest in Group IV. In histopathology, severe degeneration in liver and kidney was observed in Group II animals. These degrading changes were seen to be reduced greatly in Group III animals. The results suggested that omega-3 fatty acid might attenuate HgCI2-induced toxicity by improving antioxidant status and acute phase response in mice.

Pyridine induction of cytochrome P450 1A1, iNOS and metallothionein in Syrian hamsters and protective effects of silymarin.

An in vivo assessment for the protective effects of silymarin for pyridine toxicity was investigated through cytochrome P450 isoform CYP1A1 and inducible nitric oxide synthase (iNOS) activity prevention. Moreover, the effect of pyridine-induced oxidative stress on metallothionein I-II (MT), a scavenger of oxygen-derived free radicals, was investigated. Forty Syrian hamsters were allocated into 4 groups. Syrian hamsters were dosed with pyridine (400mg/kg) intraperitoneally with and without silymarin (200mg/kg daily by gavage) for 4 days. Pyridine induced diffuse degeneration and necrosis of the proximal and distal renal tubular cells; cloudy swelling, necrosis and hepatocellular atypia of the liver; and degenerative changes in the myocardium. The degree of pathological alterations was less severe with simultaneous silymarin application. CYP1A1, iNOS and MT expression levels were elevated in liver, kidney and heart in response to acute pyridine toxicity. Silymarin application abolished or significantly suppressed the induction of CYP1A1, iNOS and MT expressions in liver, kidney and heart of the pyridine-treated Syrian hamsters. Enhanced synthesis of MT by pyridine possibly implies a purposive cellular response to prevent damage caused by oxygen radicals. However, silymarin significantly reduced the oxidative-stress-inducing effect of pyridine as reflected by decreased synthesis of MT. These results suggest that through oxidant generation, pyridine may cause alteration of the metabolic ways, including nitric oxide-mediated CYP1A1 activity.

Hepatoprotective effect of L-carnitine against acute acetaminophen toxicity in mice.

L-carnitine is a cofactor in the transfer of long-chain fatty acid allowing the beta-oxidation of fatty acid in the mitochondria. It is also a known antioxidant with protective effects against lipid peroxidation. In this study, hepatoprotective effect of L-carnitine was investigated against acetaminophen (AA)-induced liver toxicity where mitochondrial dysfunction and oxidative stress are thought to be involved in AA hepatotoxicity. Sixty-four Balb/C mice were divided into eight groups. Mice were dosed with single-AA injection (500 mg/kg via the intra peritoneal route) with or without L-carnitine (500 mg/kg for 5 days starting 5 days before AA injection via intra peritoneal route) and sampled at 4, 8 and 24 h following AA injection. AA increased serum AST, ALT, total sialic acid (TSA) and MDA as well as tissue TSA and MDA levels significantly with the highest increase observed at 4 h, but there was a decrease in blood and tissue GSH level. Administration of L-carnitine significantly reduced AA-induced elevations in AST, ALT, TSA and MDA concentrations and increased GSH levels at all sampling points. AA also induced necrosis, hyperemia, sinusoidal congestion and hemorrhage with time-dependent increase in severity, but the degree of necrosis and histopathologic alterations were most severe at 24 h following AA administration. However, the degree of pathologic alterations was less severe with simultaneous L-carnitine application. These results suggest that AA results in oxidative damage in the liver with an acute effect. L-carnitine also has a prominent protective effect against AA toxicity and may be of therapeutic value in the treatment of AA-induced hepatotoxicity.