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Serum paraoxonase (PON1) status and ox-LDL and homocysteine concentrations in hemodialysis patients
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Abstracts
estrogen and progesterone, imaging techniques should be used for concrete solution. Keywords: Secondary amenorrhoea , LH, FSH, Prolactin, LH: FSH ratio doi:10.1016/j.clinbiochem.2011.08.127
E Poster — [A-10-925-1] Diabetes mellitus abolishes the cardioprotective effect of ischemic postconditioning against ischemia/reperfusion injury in rat: Role of lipid peroxidation Reza Badalzadeha, Mustafa Mohammadib, Moslem Najafic a Talented student office, Student Research Committee, Mashhad, Iran b Department of Physiology c Department of Pharmacology E-mail address: [email protected] (R. Badalzadeh) Introduction: The interaction of diabetes with cardioprotection by ischemic-postconditioning (IPostC) in ischemia/reperfusion (I/R) injury remains unclear. The aim of this study was to investigate the cardioprotective effect of IPostC against I/R injury in normal and diabetic rats and the role of lipid peroxidation in this case. Methods: Wistar rats (250–300 g) were divided into four groups (control, control + IPostC, diabetic, diabetic + IPostC). Diabetes was induced by single injection of streptozotocin (50 mg/kg,ip). After 8 weeks, the hearts of animals were subjected to 30 min regional ischemia (by occluding the left anterior descending coronary artery) followed by 45 min reperfusion. IPostC protocol was three-cycles of 30 s I/R immediately at the onset of reperfusion. Creatine-kinase (CK) release into coronary effluent was assessed as a marker of injury. The level of malondialdehyde (MDA) in myocardial homogenate was analyzed as a marker of lipid peroxidation. All enzymatic measurements were accomplished using commercially kits and spectrophotometery. Results: IPostC significantly reduced myocardial CK release in reperfusion phase in non-diabetic animals (12 ± 4 in control + IPostC vs 28± 5 U/L in control groups, p < 0.05) but it failed to affect the CK level of diabetic hearts (13 ± 3 in diabetic + IPostC vs 14 ± 3 U/L in diabetic groups). In addition, the level of MDA was not modified by IPostC in diabetic rats (5.9 ± 1 vs 7.7 ± 2 nmol/ml). However, IPostC in non-diabetic (control) groups significantly reduced the MDA level (2.6 ± 0.4 vs 5.2 ± 0.3 nmol/ml, p < 0.05). Conclusion: The finding of present study indicated for the first time that IpostC with three cycles of 30 s I/R fails to protect the diabetic myocardium against I/R injury and the greater oxidative stress in diabetic condition may play a role in this field. Keywords: Postconditioning, Cardioprotection, Diabetes mellitus, Reperfusion injury doi:10.1016/j.clinbiochem.2011.08.128
E Poster – [A-10-927-2] Methimazole – induced hypothyroidism during lactation affects brain nitric oxide levels in offspring rats Hosseini Mahmouda, Dastghaib Samaneh Sadata, Nahrevanian Hosseina, Farrokhi Ismaeilb a Department of Parasitology, Pasteur Institute of Iran, Tehran, Iran b Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran E-mail address: [email protected] (H. Mahmoud) Introduction: There are many reports showing a significant role for thyroid hormones in development and maturation of mammalian
central nervous system. The role of nitric oxide (NO) in neurogenesis has been reported. This study aimed to investigate the effect of hypothyroidism during lactation on NO metabolites in hippocampus as well as plasma samples of offspring rats. Methods: The animals were divided into two groups and treated for 60 days from the first day of lactation period. Group 1 (control) received tap drinking water while in group 2, 0.03% methimazole was added to drinking water. Samples of blood were collected in order to measure metabolites and thyroxine level. The offspring were then sacrificed and hippocampi were removed for measuring NO2 and NO3 in tissue. Results: Plasma thyroxine level in offspring of methimazole group was lower than control group (P< 0.01). There was no significant difference in the level of NO metabolites in plasma samples between the two groups however, significantly higher NO metabolites levels in hippocampus of group 2 were observed comparing with group1 (P< 0.05). Conclusion: These results suggest that increased nitric oxide in hippocampus may have a role in CNS damage due to hypothyroidism, though the exact mechanism needs to be more investigated. Keywords: Hypothyroidism, Lactation, Nitric Oxide, Offspring doi:10.1016/j.clinbiochem.2011.08.129
E Poster – [A-10-930-1] Serum paraoxonase (PON1) status and ox-LDL and homocysteine concentrations in hemodialysis patients Mahrooz Abdolkarim, Shaygani Shahruz, Gohari Ghorban, Zargari Mehryar, Seddighi Omid Department of Clinical Biochemistry and Genetics, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran E-mail address: [email protected] (M. Abdolkarim) Introduction: Atherosclerotic events are the leading causes of mortality in hemodialysis (HD) patients. Serum paraoxonase (PON1) is recognized as an antioxidant and antiatherogenic enzyme. Oxidized-low density lipoprotein (ox-LDL) and homocysteine are associated with an increased risk of cardiovascular diseases. In the current study, PON1 activity, total homocysteine and ox-LDL were assessed in HD patients to compare values of these parameters with control subjects and to determine the relationship between them. Materials and methods: Arylesterase activity of PON1 was measured spectrophotometrically using synthetic substrate of phenylacetate in 28 cases before and after of dialysis and 23 control subjects. Total homocysteine and ox-LDL levels were determined by ELISA method. Results: Ox-LDL (92.44 ± 5.58 vs 64.03 ± 5.92 U/L) levels were significantly increased in HD patients (p = 0.001). Homocysteine levels were higher in these patients (11.95 ± 2.61 vs 9.93 ± 3.03 μmol/ L). There were no significant changes in PON1 activity between patients and controls (50.61 ± 3.03 vs 47.24 ± 5.33 μmol/min/ml). Ox-LDL levels positively correlated with homocysteine levels. PON1 activity inversely correlated with ox-LDL and homocysteine levels. Conclusion: This study showed the further evidence that ox-LDL and homocysteine specially ox-LDL may play a role in pathologic mechanisms that may contribute to atherogenesis in HD patients and suggest that similar study involving larger samples need to be done to elucidate efficiently role of PON1 in hemodialysis. Keywords: Serum paraoxonase, ox-LDL, Homocysteine, Hemodialysis, Atherosclerosis doi:10.1016/j.clinbiochem.2011.08.1067
Abstracts
estrogen and progesterone, imaging techniques should be used for concrete solution. Keywords: Secondary amenorrhoea , LH, FSH, Prolactin, LH: FSH ratio doi:10.1016/j.clinbiochem.2011.08.127
E Poster — [A-10-925-1] Diabetes mellitus abolishes the cardioprotective effect of ischemic postconditioning against ischemia/reperfusion injury in rat: Role of lipid peroxidation Reza Badalzadeha, Mustafa Mohammadib, Moslem Najafic a Talented student office, Student Research Committee, Mashhad, Iran b Department of Physiology c Department of Pharmacology E-mail address: [email protected] (R. Badalzadeh) Introduction: The interaction of diabetes with cardioprotection by ischemic-postconditioning (IPostC) in ischemia/reperfusion (I/R) injury remains unclear. The aim of this study was to investigate the cardioprotective effect of IPostC against I/R injury in normal and diabetic rats and the role of lipid peroxidation in this case. Methods: Wistar rats (250–300 g) were divided into four groups (control, control + IPostC, diabetic, diabetic + IPostC). Diabetes was induced by single injection of streptozotocin (50 mg/kg,ip). After 8 weeks, the hearts of animals were subjected to 30 min regional ischemia (by occluding the left anterior descending coronary artery) followed by 45 min reperfusion. IPostC protocol was three-cycles of 30 s I/R immediately at the onset of reperfusion. Creatine-kinase (CK) release into coronary effluent was assessed as a marker of injury. The level of malondialdehyde (MDA) in myocardial homogenate was analyzed as a marker of lipid peroxidation. All enzymatic measurements were accomplished using commercially kits and spectrophotometery. Results: IPostC significantly reduced myocardial CK release in reperfusion phase in non-diabetic animals (12 ± 4 in control + IPostC vs 28± 5 U/L in control groups, p < 0.05) but it failed to affect the CK level of diabetic hearts (13 ± 3 in diabetic + IPostC vs 14 ± 3 U/L in diabetic groups). In addition, the level of MDA was not modified by IPostC in diabetic rats (5.9 ± 1 vs 7.7 ± 2 nmol/ml). However, IPostC in non-diabetic (control) groups significantly reduced the MDA level (2.6 ± 0.4 vs 5.2 ± 0.3 nmol/ml, p < 0.05). Conclusion: The finding of present study indicated for the first time that IpostC with three cycles of 30 s I/R fails to protect the diabetic myocardium against I/R injury and the greater oxidative stress in diabetic condition may play a role in this field. Keywords: Postconditioning, Cardioprotection, Diabetes mellitus, Reperfusion injury doi:10.1016/j.clinbiochem.2011.08.128
E Poster – [A-10-927-2] Methimazole – induced hypothyroidism during lactation affects brain nitric oxide levels in offspring rats Hosseini Mahmouda, Dastghaib Samaneh Sadata, Nahrevanian Hosseina, Farrokhi Ismaeilb a Department of Parasitology, Pasteur Institute of Iran, Tehran, Iran b Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran E-mail address: [email protected] (H. Mahmoud) Introduction: There are many reports showing a significant role for thyroid hormones in development and maturation of mammalian
central nervous system. The role of nitric oxide (NO) in neurogenesis has been reported. This study aimed to investigate the effect of hypothyroidism during lactation on NO metabolites in hippocampus as well as plasma samples of offspring rats. Methods: The animals were divided into two groups and treated for 60 days from the first day of lactation period. Group 1 (control) received tap drinking water while in group 2, 0.03% methimazole was added to drinking water. Samples of blood were collected in order to measure metabolites and thyroxine level. The offspring were then sacrificed and hippocampi were removed for measuring NO2 and NO3 in tissue. Results: Plasma thyroxine level in offspring of methimazole group was lower than control group (P< 0.01). There was no significant difference in the level of NO metabolites in plasma samples between the two groups however, significantly higher NO metabolites levels in hippocampus of group 2 were observed comparing with group1 (P< 0.05). Conclusion: These results suggest that increased nitric oxide in hippocampus may have a role in CNS damage due to hypothyroidism, though the exact mechanism needs to be more investigated. Keywords: Hypothyroidism, Lactation, Nitric Oxide, Offspring doi:10.1016/j.clinbiochem.2011.08.129
E Poster – [A-10-930-1] Serum paraoxonase (PON1) status and ox-LDL and homocysteine concentrations in hemodialysis patients Mahrooz Abdolkarim, Shaygani Shahruz, Gohari Ghorban, Zargari Mehryar, Seddighi Omid Department of Clinical Biochemistry and Genetics, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran E-mail address: [email protected] (M. Abdolkarim) Introduction: Atherosclerotic events are the leading causes of mortality in hemodialysis (HD) patients. Serum paraoxonase (PON1) is recognized as an antioxidant and antiatherogenic enzyme. Oxidized-low density lipoprotein (ox-LDL) and homocysteine are associated with an increased risk of cardiovascular diseases. In the current study, PON1 activity, total homocysteine and ox-LDL were assessed in HD patients to compare values of these parameters with control subjects and to determine the relationship between them. Materials and methods: Arylesterase activity of PON1 was measured spectrophotometrically using synthetic substrate of phenylacetate in 28 cases before and after of dialysis and 23 control subjects. Total homocysteine and ox-LDL levels were determined by ELISA method. Results: Ox-LDL (92.44 ± 5.58 vs 64.03 ± 5.92 U/L) levels were significantly increased in HD patients (p = 0.001). Homocysteine levels were higher in these patients (11.95 ± 2.61 vs 9.93 ± 3.03 μmol/ L). There were no significant changes in PON1 activity between patients and controls (50.61 ± 3.03 vs 47.24 ± 5.33 μmol/min/ml). Ox-LDL levels positively correlated with homocysteine levels. PON1 activity inversely correlated with ox-LDL and homocysteine levels. Conclusion: This study showed the further evidence that ox-LDL and homocysteine specially ox-LDL may play a role in pathologic mechanisms that may contribute to atherogenesis in HD patients and suggest that similar study involving larger samples need to be done to elucidate efficiently role of PON1 in hemodialysis. Keywords: Serum paraoxonase, ox-LDL, Homocysteine, Hemodialysis, Atherosclerosis doi:10.1016/j.clinbiochem.2011.08.1067