The effect of Hippophae rhamnoides L. extract on acrylamideinduced brain injury in rats.

PURPOSE: Reactive oxygen species (ROS), interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α) have been shown in the pathogenesis of acrylamide neurotoxicity. Hippophae rhamnoides L. extract (HRE) has a cytoprotective effect by stabilizing the production of ROS, IL-1ß and TNF-α. The objective of the article was to investigate the effect of HRE on acrylamide-induced brain damage in rats biochemically and histopathologically. METHODS: To the HRE+acrylamide only (ACR) group (n=6) of the animals, HRE was administered orally at a dose of 50 mg / kg into the stomach by gavage. The same volume of solvent (olive oil) was administered orally to the ACR (n=6) and healthy (HG) (n=6) groups. One hour after HRE administration, acrylamide was given orally at a dose of 20 mg/kg to HRE+ACR and ACR groups in the same way. This procedure was repeated once a day for 30 days. At the end of this period, brain tissues extracted from animals killed with 50 mg/kg thiopental anesthesia were examined biochemically and histopathologically. RESULTS: It has been shown that HRE prevents the increase of malondialdehyde (MDA), myeloperoxidase (MPO), IL-1ß and TNF-α with acrylamide and the decrease of total glutathione (tGSH) and glutathione reductase (GSHRd) levels in brain tissue. CONCLUSIONS: HRE may be useful in the treatment of acrylamide-induced neurotoxicity.

The effect of Hippophae rhamnoides L. extract on acrylamideinduced brain injury in rats

ABSTRACT Purpose: Reactive oxygen species (ROS), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) have been shown in the pathogenesis of acrylamide neurotoxicity. Hippophae rhamnoides L. extract (HRE) has a cytoprotective effect by stabilizing the production of ROS, IL-1β and TNF-α. The objective of the article was to investigate the effect of HRE on acrylamide-induced brain damage in rats biochemically and histopathologically. Methods: To the HRE+acrylamide only (ACR) group (n=6) of the animals, HRE was administered orally at a dose of 50 mg / kg into the stomach by gavage. The same volume of solvent (olive oil) was administered orally to the ACR (n=6) and healthy (HG) (n=6) groups. One hour after HRE administration, acrylamide was given orally at a dose of 20 mg/kg to HRE+ACR and ACR groups in the same way. This procedure was repeated once a day for 30 days. At the end of this period, brain tissues extracted from animals killed with 50 mg/kg thiopental anesthesia were examined biochemically and histopathologically. Results: It has been shown that HRE prevents the increase of malondialdehyde (MDA), myeloperoxidase (MPO), IL-1β and TNF-α with acrylamide and the decrease of total glutathione (tGSH) and glutathione reductase (GSHRd) levels in brain tissue. Conclusions: HRE may be useful in the treatment of acrylamide-induced neurotoxicity.

The effect of lifestyle change and metformin therapy on serum arylesterase and paraoxonase activity in obese children.

AIM: Obesity is known to be associated with many diseases in the long and short terms. Elevated oxidative stress contributes to the development of such obesity-related diseases as dyslipidemia, diabetes mellitus and hypertension. Levels of the endogenous antioxidants paraoxonase and arylesterase have been shown to decrease in such diseases. The purpose of this study was to investigate whether or not changes in lifestyle and metformin therapy would affect serum paraoxonase and arylesterase levels. MATERIALS AND METHODS: The study was performed with 25 overweight, 26 obese and 25 morbidly obese patients aged 6-15 years as well as 27 healthy children. Serum paraoxonase (PON1) and arylesterase (ARE) activity levels and total cholesterol, triglyceride, low-density protein, high-density protein, very low-density protein, glucose, aspartate amino transferase and alanine amino transferase levels were measured. Enrolled patients were assessed at initial presentation and again at 6 months. No procedure was performed in the control group, while the overweight, obese and morbidly obese groups were recommended diet and exercise and given metformin therapy (insulin-resistant subjects only). RESULTS: Serum PON1 activity levels in patients with metabolic syndrome were significantly lower than those in individuals without metabolic syndrome (p<0.05), while lipid concentrations were significantly higher (p<0.05). Metabolic syndrome patients had higher serum glucose, total cholesterol, low-density protein, very low-density protein and triglyceride values compared to those of the control group but significantly lower high-density protein values (p<0.05). No difference was determined between the groups in terms of PON1 and ARE levels following diet and exercise and metformin therapy. CONCLUSION: Measurement of PON1 and ARE enzyme levels may be useful in monitoring the effectiveness of treatment aimed at reducing oxidative stress in obese children.

Damage induced by paracetamol compared with N-acetylcysteine.

BACKGROUND: This study investigated the effect of thiamine pyrophosphate (TPP) on oxidative liver damage induced in rats with high-dose paracetamol. METHODS: Rats for this experiment were divided into the following groups: healthy control, paracetamol control, thiamine + paracetamol, TPP + paracetamol, and N-acetylcysteine + paracetamol. Oxidant and antioxidant parameters and liver function test levels were compared between the groups. RESULTS: The results show that TPP and N-acetylcysteine with paracetamol equally prevented a rise in oxidants such as malondialdehyde and nitric oxide. They also prevented a decrease in enzymatic and nonenzymatic antioxidants such as glutathione, glutathione peroxidase, glutaredoxin, glutathione S-transferase, superoxide dismutase, and catalase in the rat liver. CONCLUSION: Thiamine pyrophosphate and N-acetylcysteine had a similar positive effect on oxidative damage caused by paracetamol hepatotoxicity. These findings show that TPP may be beneficial in paracetamol hepatotoxicity.

Bilateral ovarian ischemia/reperfusion injury and treatment options in rats with an induced model of diabetes.

OBJECTIVES: This study investigated the effects of melatonin, famotidine, mirtazapine, and thiamine pyrophosphate on ischemia/reperfusion (I/R) injury in diabetic rats and evaluated oxidant and antioxidant marker measurement results. It also examined the effects of the drugs aimed at preventing infertility that may result from I/R injury. MATERIALS AND METHODS: Diabetic rats were divided into a control group (IRC) to be exposed to I/R, an ovarian I/R + 2.2 mg/kg melatonin (IRML) group, an ovarian I/R + famotidine (IRFA) group, an ovarian I/R + 20 mg/kg mirtazapine (IRMR) group, an ovarian I/R + 20 mg/kg thiamine pyrophosphate (IRTP) group, and a sham operation (SO) group. RESULTS: In the control group exposed to I/R, the levels of the oxidant parameters Malondialdehyde (MDA) and Myeloperoxidase (MPO) were significantly higher compared with the SO group, while the levels of the antioxidant parameters glutathione (GSH), Glutathione peroxidase (GPO), Glutathione reductase (GSHRd), Glutathione S - transferase (GST), and Superoxide dismutase (SOD) were significantly lower. Melatonin, famotidine, mirtazapine, and thiamin pyrophosphate prevented a rise in oxidant parameters and a decrease in antioxidants in ovarian tissue exposed to I/R. However, apart from thiamin pyrophosphate, none of the drugs were able to prevent infertility caused by I/R injury. CONCLUSION: Prevention of ovarian I/R injury-related infertility in rats with induced diabetes is not through antioxidant activity. Thiamine pyrophosphate prevents infertility through an as yet unknown mechanism. This study suggests that thiamine pyrophosphate may be useful in the prevention of I/R-related infertility in diabetics.

Protective effect of nimesulide against hepatic ischemia/reperfusion injury in rats: effects on oxidant/antioxidants, DNA mutation and COX-1/COX-2 levels.

BACKGROUND: Nimesulide is a pharmacological agent and selective COX-2 inhibitor. It has anti-inflammatory, analgesic and antipyretic properties. The purpose of this study was to investigate the effect of nimesulide on oxidant/antioxidant, DNA mutation and COX-1/COX-2 activities in rat liver tissue with induced ischemia/reperfusion (I/R). METHODS: Before the experiment, rats were divided into four groups; liver ischemia/reperfusion (LIR), 50mg/kg nimesulide+liver ischemia/reperfusion (NLIR50), 100mg/kg nimesulide+liver ischemia/reperfusion (NLIR100) and a control group to be given a sham operation (SG). Malondialdehyde (MDA), total glutathione (GSH) levels and myeloperoxidase (MPO), COX-1/COX-2 enzyme activities and DNA damage product level results from liver tissues and serum AST and ALT levels were determined. The data obtained were compared with the results from the liver ischemia/reperfusion and sham operation groups. RESULTS: MDA levels, MPO and COX-2 activities and products of DNA injury were significantly lower in the groups given nimesulide, and particularly the NLIR100 group, compared to the LIR group (p<0.05), while tGSH levels were significantly higher (p<0.05). There was no significant difference between the NLIR50 and NLIR100 groups and the LIR group in terms of COX-1 levels (p>0.05). AST and ALT levels were significantly lower in the other groups compared to the LIR group (p<0.05). CONCLUSIONS: Nimesulide at 100mg/kg prevented oxidative liver damage induced with I/R significantly better than at a dose of 50mg/kg. These experimental findings indicate that nimesulide may be useful in the treatment of hepatic I/R damage.

Benefits of the antioxidant and anti-inflammatory activity of etoricoxib in the prevention of ovarian ischemia/reperfusion injury induced experimentally in rats.

AIM: This study is a biochemical investigation of the effect of etoricoxib, a selective cyclooxygenase (COX)-2 inhibitor, on ischemia/reperfusion (I/R) injury experimentally induced in rat ovaries. METHODS: Experimental animals were divided into four groups: (i) ovarian ischemia/reperfusion (IRG); (ii) 30 mg/kg etoricoxib + ovarian ischemia/reperfusion (EIRG-30); (iii) 60 mg/kg etoricoxib + ovarian ischemia/reperfusion (EIRG-60); and (iv) a sham operation (SG) control group. RESULTS: The results showed levels of malondialdehyde in the IRG, EIRG-30, EIRG-60 and SG group ovarian tissue of 20.2 ± 3.4, 11.2 ± 3.2, 5.5 ± 1.9 and 3.8 ± 1.5 µmol/g protein, respectively. Myeloperoxidase activity for these groups was 24.2 ± 6.7, 13 ± 2.4, 4 ± 1.8 and 3.5 ± 1.9 U/g protein, and total glutathione levels were 1.6 ± 0.8, 4.5 ± 1.9, 6.5 ± 1.9 and 7.5 ± 2.4 nmol/g protein, respectively. COX-1 activity in IRG, EIRG-30, EIRG-60 and SG group rat ovarian tissue was 5.0 ± 2.8, 12.2 ± 2.4, 16.7 ± 2.8 and 17.5 ± 4.7 U/mg protein, and COX-2 activity was 18.3 ± 2.7, 3.5 ± 1, 1.8 ± 0.7 and 0.7 ± 0.3 U/mg protein, respectively. CONCLUSION: Etoricoxib prevented oxidative damage induced with I/R in rat ovarian tissue. This property of etoricoxib suggests that it can be clinically beneficial in the prevention of damage that may arise with reperfusion by detorsion for the protection of the ovaries against torsion.

Antioxidant status in blood of obese children: the relation between trace elements, paraoxonase, and arylesterase values.

Obesity is known to lead to complications involving several systems. The basic mechanism in obesity-related complications is chronic inflammation and increased oxidative stress. Trace element levels in obese children may vary due to poor nutritional habits. The purpose of this study was to investigate the relation between serum paraoxonase (PON1) and arylesterase (ARE) levels, markers of the oxidant-antioxidant balance in the body, and serum zinc (Zn), copper (Cu), manganese (Mn), and selenium (Se) concentrations in obese children. Fifty-seven overweight patients aged 6-17 and 48 age- and sex-matched healthy children were included in the study. Serum PON1 and ARE activity levels were measured, together with Cu, Zn, Mn, Se, total cholesterol, triglyceride, low-density lipoprotein, high-density lipoprotein, very low-density lipoprotein, glucose, aspartate amino transferase, and alanine amino transferase levels. PON1 and ARE activity levels were significantly lower in obese patients compared to those in healthy individuals (P < 0.05). Various changes were determined in Cu, Zn, Mn, and Se levels between the study and control groups (P < 0.05). In terms of the relation between trace elements and PON1 and ARE levels, a significant positive correlation was determined between serum Se and PON1 levels in the study group (P < 0.05, r = 0.31). No significant correlation was determined between other trace element levels and PON1 and ARE levels (P > 0.05). In conclusion, the detection in our study of a positive correlation between Se and PON1 levels in obese children may be significant in terms of showing a relation between Se and antioxidant systems in obese children.

Psoriasis vulgaris and autoimmune polyendocrine syndrome type I: a case report.

Autoimmune polyglandular syndrome (APS) is a rarely diagnosed condition characterized by a combination of two or more organ-specific autoimmune diseases and divided into a very rare juvenile (APS type I) and a relatively common adult type (APS II-IV). The major components of APS-I are hypoparathyroidism, adrenal failure, and mucocutaneous candidiasis. In addition to the classic triad, many other autoimmune diseases could be associated with the syndrome. We report an adolescent patient with psoriasis vulgaris and APS-I.

The suppression of endogenous adrenalin in the prolongation of ketamine anesthesia.

This study investigated whether or not the anesthetic effect of ketamine in rats is dependent on adrenal gland hormones. The study was performed on two main rat groups, intact and adrenalectomized. Rat were divided into subgroups and given appropriate doses of ketamine, metyrapone or metyrosine. Durations of anesthesia in the groups were then recorded. Endogenous catecholamine levels were measured in samples taken from peripheral blood. This experimental results showed that ketamine did not induce anesthesia in intact rats at doses of 15 or 30mg/kg, and that at 60mg/kg anesthesia was established for only 11min. However, ketamine induced significant anesthesia even at a dose of 30mg/kg in animals in which production of endogenous catecholamine (adrenalin, noradrenalin dopamine) was inhibited with metyrosine at a level of 45-47%. Ketamine at 60mg/kg in animals in which endogenous catecholamine was inhibited at a level of 45-47% established anesthesia for 47.6min. However, ketamine at 30 and 60mg/kg induced longer anesthesia in adrenalectomized rats with higher noradrenalin and dopamine levels but suppressed adrenalin production. Adrenalin plays an important role in the control of duration of ketamine anesthesia, while noradrenalin, dopamine and corticosterone have no such function. If endogenous adrenalin is suppressed, ketamine can even provide sufficient anesthesia at a 2-fold lower dose. This makes it possible for ketamine to be used in lengthy surgical procedures.

Effects of thiamine and thiamine pyrophosphate on epileptic episode model established with caffeine in rats.

This study examines the effect of thiamine (TH) and thiamine pyrophosphate (TPP) on epileptic episode model induced in rats with caffeine. Animals were divided into groups and given TH or TPP at doses of 10, 30 or 50mg/kg intraperitoneally. Subsequently, all animal groups were injected intraperitoneally with caffeine at a dose of 300mg/kg. Time of onset of epileptic episode was recorded, and the latent period was calculated in seconds. At the end of the experiment, tGSH and MDA levels and SOD and MPO enzyme activities in extracted brain tissues were measured. Latent period duration in rats in the control group was 134±3.2s, compared to 144±13.9, 147±14.5 and 169±15.1s, respectively, in the TH10, TH30 and TH50 groups and 184±8.54, 197±9.1, 225±8.37s, respectively, in the TPP10, TPP30 and TPP50 groups. Latent period duration was 236±6.7 in the diazepam group. Oxidant products were significantly lower in the TPP10, TPP30, TPP50 and diazepam groups compared to the control group (P<0.05), while SOD activity and tGSH levels were significantly higher (P<0.05). There was no significant difference between the TH10, TH30, TH50 groups and the control group in terms of oxidant and antioxidant levels (P>0.05). In conclusions, TPP, especially at a dose of 50mg/kg, significantly prolonged the latent period from administration of caffeine to time of episode and prevented oxidative damage.

Thyroid functions and trace elements in pediatric patients with exogenous obesity.

Obesity is a multifactorial disease developing following impairment of the energy balance. The endocrine system is known to be affected by the condition. Serum thyroid hormones and trace element levels have been shown to be affected in obese children. Changes in serum thyroid hormones may result from alterations occurring in serum trace element levels. The aim of this study was to evaluate whether or not changes in serum thyroid hormone levels in children with exogenous obesity are associated with changes in trace element levels. Eighty-five children diagnosed with exogenous obesity constituted the study group, and 24 age- and sex-matched healthy children made up the control group. Serum thyroid stimulating hormone (TSH), free thyroxine (fT4), free triiodothyronine (fT3), thyroglobulin (TG), selenium (Se), zinc (Zn), copper (Cu), and manganese (Mn) levels in the study group were measured before and at the third and sixth months of treatment, and once only in the control group. Pretreatment fT4 levels in the study group rose significantly by the sixth month (p = 0.006). Zn levels in the patient group were significantly low compared to the control group (p = 0.009). Mn and Se levels in the obese children before and at the third and sixth months of treatment were significantly higher than those of the control group (p = 0.001, p = 0.001). In conclusion, fT4, Zn, Cu, Mn, and Se levels are significantly affected in children diagnosed with exogenous obesity. The change in serum fT4 levels is not associated with changes in trace element concentrations.

Serum vitamin D levels in children with recurrent otitis media.

The aims of this study were to evaluate serum vitamin D levels in cases of recurrent otitis media and investigate the effect of vitamin D therapy on the risk of re-occurrence of the disease. This prospective study was performed by comparing serum vitamin D levels in children with recurrent otitis media and healthy children. Eighty-four children between 1 and 5 years of age and diagnosed with recurrent otitis media were enrolled as the study group. One hundred-and-eight healthy children with similar demographic characteristics were enrolled as the control group. Patients were divided into groups according to their serum 25(OH) vitamin D levels. In patients with low initial serum vitamin D levels, vitamin D therapy was administered in addition to conventional treatment for otitis media. Mean serum 25(OH) vitamin D level in the study group was 11.4 ± 9.8 ng/mL Serum 25(OH) vitamin D levels were below 20 ng/mL in 69 % (n = 58) of cases in this group. In the control group, mean serum 25(OH) vitamin D level was 29.2 ± 13.9 ng/mL and was below 20 ng/mL in 30 % (n = 32) of cases. Comparison of serum 25(OH) vitamin D levels and PTH in the study and control groups revealed a statistically significant difference (p < 0.05). Treatment was initiated in cases diagnosed with vitamin D deficiency, and patients were followed up in due course. The only episodes detected over the course of 1-year follow-up were one attack in five patients and two attacks in two. We believe that co-administration of supplementary vitamin D together with conventional treatments is appropriate in the management of upper respiratory infections such as otitis media.

The protective effect of thiamine pyrophosphate, but not thiamine, against cardiotoxicity induced with cisplatin in rats.

This study investigated the effect of thiamine pyrophosphate on oxidative damage associated with cardiotoxicity caused by cisplatin (CIS), an antineoplastic agent, in rats, and compared this with thiamine. Animals used in the study were divided into four groups of 6 rats each. These represented a control group receiving 5 mg/kg of CIS, study groups receiving 20 mg/kg of thiamine pyrophosphate plus 5 mg/kg of cisplatin (CTPG) or 20 mg/kg of thiamine plus 5 mg/kg of cisplatin and a healthy (H) group. All doses were administered intraperitoneally once a day for 14 days. Malondialdehyde, total glutathione and products of DNA injury results were similar in the CTPG and H groups (p > 0.05). Creatinine kinase, creatine kinase MB and troponin 1 levels were similar in the CTPG and H groups (p > 0.05). Thiamine pyrophosphate prevented CIS-associated oxidative stress and heart injury, whereas thiamine did not prevent these.

An examination of the mutual effects of valproic acid, carbamazepine, and phenobarbital on 25-hydroxyvitamin D levels and thyroid function tests.

BACKGROUND: The effects of antiepileptic drugs (AEDs) on bone metabolism and the endocrine system are not fully known, and publications on the subject are inconsistent. OBJECTIVE: The study aimed to examine the mutual effects of valproic acid (VPA), carbamazepine (CBZ), and phenobarbital (PB)-AEDs frequently used in childhood-on bone mineral metabolism and thyroid function tests. PATIENTS AND METHODS: Children monitored with a diagnosis of idiopathic epilepsy by the pediatric neurology clinic, using AEDs for at least 6 months and with episodes under control, were included in the study. Patients were divided into groups on the basis of the drugs used. Thyroid function tests and 25-hydroxyvitamin D or 25(OH)D levels were measured from blood specimens. The data obtained were then compared with those of the control group. RESULTS: A significantly high level of subclinical hypothyroidism was seen in patients using VPA (p < 0.001). There was no significant difference between any of the three study groups and the control group in terms of 25(OH)D (p > 0.05). CONCLUSIONS: Pediatric patients using AEDs, particularly VPA, should be monitored for subclinical hypothyroidism. VPA, CBZ, and PB have no effect on vitamin D levels.

Vitamin D levels in children diagnosed with acute otitis media.

OBJECTIVE: To investigate the relationship between Vitamin D deficiency and acute otitis media infection. METHODS: The randomised, single-blind, case-control study was conducted at the Paediatric Department of Ataturk University, Erzurum, Turkey, from January to April 2010. It comprised ambulatory children diagnosed with acute otitis media and healthy controls. The subjects were divided into groups according to their serum 25-hydroxy vitamin D levels. SPSS 18 was used for statistical analysis. RESULTS: Of the 169 subjects in the study, 88(52%) were the cases and 81(48%) were controls. The mean age of the cases was 6.21±3.4 years, and 6.18±3.12 years for the controls (p<0.951). Serum 25-hydroxy vitamin D levels in the cases and controls were 20.6±10.2 ng/mL and 23.8±10.3 ng/mL (p<0.05). There was no statistically significant difference between the groups in terms of parathormone and calcium levels (p>0.05). CONCLUSION: Serum 25-hydroxy vitamin D levels being significantly lower in children diagnosed with acute otitis media compared to the controls in two otherwise similar groups suggests that Vitamin D deficiency plays a role in otitis media infection.

The effect of thiamine and thiamine pyrophosphate on oxidative liver damage induced in rats with cisplatin.

The aim of this study was to investigate the effect of thiamine and thiamine pyrophosphate (TPP) on oxidative stress induced with cisplatin in liver tissue. Rats were divided into four groups; thiamine group (TG), TPP + cisplatin group (TPG), healthy animal group (HG), and cisplatin only group (CG). Oxidant and antioxidant parameters in liver tissue and AST, ALT, and LDH levels in rat sera were measured in all groups. Malondialdehyde levels in the CG, TG, TPG, and HG groups were 11 ± 1.4, 9 ± 0.5, 3 ± 0.5, and 2.2 ± 0.48 µ mol/g protein, respectively. Total glutathione levels were 2 ± 0.7, 2.8 ± 0.4, 7 ± 0.8, and 9 ± 0.6 nmol/g protein, respectively. Levels of 8-OH/Gua, a product of DNA damage, were 2.7 ± 0.4 pmol/L, 2.5 ± 0.5, 1.1 ± 0.3, and 0.9 ± 0.3 pmol/L, respectively. A statistically significant difference was determined in oxidant/antioxidant parameters and AST, ALT, and LDH levels between the TPG and CG groups (P < 0.05). No significant difference was determined between the TG and CG groups (P > 0.05). In conclusion, cisplatin causes oxidative damage in liver tissue. TPP seems to have a preventive effect on oxidative stress in the liver caused by cisplatin.

Congenital absence of the portal vein in a patient with multiple vascular anomalies.

A 15-year-old male patient accepted to emergency department with nausea, vomiting, sleepiness, and severe epigastric pain. The patient has a history of mild mental retardation since his childhood. Physical examination showed epigastric tenderness. Laboratory findings were consistent with mildly increased liver enzymes and hyperammonemia. Result of abdominal ultrasound was suboptimal due to lack of patient cooperation. Patient underwent abdominal and thoracic computed tomography (CT) examination to investigate the possible causes of hyperammonemia and liver disease. The CT scan showed the absence of portal vein with direct connection of portomesenteric system with systemic venous circulation. There were also various arterial and venous anomalies along with multiple hepatic masses. Whole anatomy of the thorax and abdomen was delineated with multiplanar reformatted images and maximum intensity projection technique. Imaging findings are consistent with Type Ib Abernethy malformation. The patient also underwent brain magnetic resonance imaging to investigate the presence of central nervous system changes due to hyperammonemia.