The effects of omega-3 fatty acids on antioxidant enzyme activities and nitric oxide levels in the cerebral cortex of rats treated ethanol.

The toxic effect of ethanol on the cerebral cortex and protective effects of omega-3 fatty acids against this neurotoxicity were investigated. Twenty eight male Wistar-albino rats were divided into 4 groups. Rats of the ethanol and ethanol withdrawal groups were treated with ethanol (6 g/kg/day) for 15 days. Animals of the ethanol+omega-3 group received omega-3 fatty acids (400 mg/kg daily) and ethanol. In rats of the ethanol group SOD activity was lower than in animals of the control group. In rats treated with omega-3 fatty acids along with ethanol SOD, activity increased. GSH-Px activity and MDA levels in animals of all groups were similar. In ethanol treated rats NO levels significantly decreased as compared to the animals of the control group (6.45±0.24 nmol/g vs 11.05±0.53 nmol/g, p.

The relationship between phthalates and obesity: serum and urine concentrations of phthalates.

BACKGROUND: A limited number of human and animal studies suggest that a relationship exists between phthalates and obesity, although this is not supported by all research. The purpose of this study was to investigate the relationship between Body Mass Index (BMI) and the levels of phthalates in human blood and urine samples. METHODS: Sixty-four overweight or 132 obese individuals (total=196) of different ages (min-max, 17-62; mean ± SD, 42.07±11.3) and genders (F:M 97:99) enrolled in the study. BMI and waist circumference were measured to diagnose obesity. Venous blood samples were taken after overnight fasting. To compare the urine phthalates among participants, single spot urine (at least 10 mL) was collected from the subject after blood samples were taken. Urine and blood phthalate concentrations were measured using gas chromatography. RESULTS: Total blood/urinary phthalate levels significantly increased in proportion to the degree of obesity. There was a high correlation between the level of total phthalates in serum and BMI (ρ=0.697, P<0.001), and between total urinary phthalate levels and BMI (ρ=0.707, P<0.001). CONCLUSIONS: This is the first study to have shown that both blood and urinary phthalates increased in proportion to BMI. The results show a strong association between obesity and phthalates.

The effect of caffeic acid phenethyl ester on isoproterenol-induced myocardial injury in hypertensive rats.

OBJECTIVE: The aim of this study is to investigate the effects of caffeic acid phenethyl ester (CAPE) on isoproterenol (ISO)-induced myocardial injury in hypertensive rats. METHODS: Rats were divided into 4 groups (n=29): Control group (n=8), L-NNA (NG-Nitro-L-arginine) group (n=8), L-NNA+ISO (L-NNA+isoproterenol) group (n=7) and L-NNA+ISO+CAPE (L-NNA+ISO + caffeic acid phenethyl ester) group (n=6). ISO (150 mg/kg/day) was given intraperitoneally (i.p.) once a day for 2 consecutive days (at the 12th and 13th days of L-NNA treatment). NG-Nitro-L-arginine (L-NNA) was given orally (25 mg/kg/day) in drinking water for 14 days. CAPE (10 µmol/kg/day) was given (i.p.) for 7 days after the first week. Systolic blood pressure (SBP) was evaluated by the tail-cuff method and biochemical analysis were performed using an autoanalyzer and a spectrophotometer. RESULTS: SBP in all L-NNA-treated groups was found to be increased at seventh day. AST and LDH levels in LNNA+ISO group were significantly increased compared to control (AST: 125±5 vs. 105±2; LDH: 861±154 vs. 571±46 U/L respectively) (p<0.05). Also, ISO caused to extensive necrosis and mononuclear cell infiltration in hypertensive rat myocardium. CAPE application reversed the enhanced AST and LDH levels as well as the extensive necrosis and the mononuclear cell infiltration in LNNA+ISO+CAPE group compared LNNA+ISO. CONCLUSION: According to our findings, it might be suggested that CAPE may be a favorable agent to protect the hypertensive myocardium from the injury induced by isoproterenol via mechanisms such as the induction of the antioxidant enzymes and the inhibition of lipid peroxidation.

Effects of paliperidone palmitate on coagulation: an experimental study.

OBJECTIVE: The aim of the present study was to examine the effects of a new antipsychotic drug paliperidone palmitate on hemogram and coagulation parameters in rats. MATERIALS AND METHODS: Experiments were performed on 22 female albino Wistar rats (8-12 weeks old). Control group was given drinking water as vehicle (0.3 mL). PAL-1 rats were given 1 mg/kg paliperidone palmitate (in 0.3 mL drinking water) by oral gavage once a day for ten days and PAL-3 rats received 3 mg/kg paliperidone palmitate (in 0.3 mL drinking water) by oral gavage for ten days. Blood samples were drawn from the heart 24 hours after the last drug dose, and hemogram and coagulation parameters were measured with automated analyzers. RESULTS: Hemogram did not change in the paliperidone treated groups compared to the controls. Factor VIII levels decreased in the PAL-1 and PAL-3 groups; and this decrease was significantly greater in the PAL-3. Factor IX levels decreased in PAL-3 rats, but its levels also increased in PAL-1 rats compared to the control. DISCUSSION: Paliperidone has led to changes in the serum levels of coagulation factors VIII and IX in rats. As a result, paliperidone may be causing thromboembolism or bleeding in a dose-independent manner.

Investigation of serum bisphenol A, vitamin D, and parathyroid hormone levels in patients with obstructive sleep apnea syndrome.

Obstructive sleep apnea syndrome (OSAS) is a common health problem, and associated with obesity, metabolic syndrome (MetS), and diabetes. Growing evidence shows that 25-hydroxyvitamin-D3 (25-OH-D) insufficiency and high parathyroid hormone (PTH) levels may be correlated to glucose intolerance, MetS, obesity, and cardiovascular abnormalities similar to OSAS. Bisphenol A (BPA) is an endocrine disruptor agent which exerts a wide variety of metabolic effects. It has estrogenic activity and its exposure may contribute to weight gain, obesity, impaired glucose metabolism, and the development of diabetes, also similar to OSAS. The aim of this study is to investigate the relationships between OSAS and serum BPA, 25-OH-D, and PTH levels. This study enrolled 128 subjects, with all of the OSAS patients having been diagnosed by polysomnography. The 128 subjects were divided into three groups: a control (n = 43), a moderate OSAS (n = 23) (AHI = 15-30), and a severe OSAS groups (n = 62) (AHI > 30). The serum BPA, 25-OH-D, and PTH levels for each subject were analyzed. 25-OH-D was lower in both OSAS groups, and PTH was higher in the OSAS groups than in the control subjects. The BPA levels were higher in the severe OSAS group than the moderate OSAS and control. There was a positive correlation between the BPA and body mass index, and a negative correlation between the 25-OH-D and BPA levels in all of the individuals. OSAS is related to high BPA and PTH levels, and low vitamin D levels. There is a positive association between BPA levels and OSAS, and the severity of OSAS. These results suggest that the BPA levels may have a role in the pathogenesis of OSAS.

Effect of tadalafil on neointimal hyperplasia in a rabbit carotid artery anastomosis model.

PURPOSE: Intimal thickening, which results from the response to arterial damage caused by therapeutic interventions or other reasons, is usually called as neointima. Neointimal hyperplasia is a main step in the pathogenesis of late-term restenosis, which is developed after vascular interventions. Reduction in nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signaling plays a substantial role in the pathogenesis of neointima formation. Phosphodiesterase V is detected in the peripheral coronary and pulmonary vascular smooth muscle cells and in the cardiac tissue. Based on the effects of phosphodiesterase V inhibitors on vascular smooth muscle cells, in the present study, the effect of tadalafil, a new member of phosphodiesterase V inhibitors, on neointimal hyperplasia was investigated in the rabbit carotid artery anastomosis model. MATERIAL AND METHOD: Fourteen male New Zealand white rabbits weighing between 2.5-3 kg, were used. The rabbits were randomly divided into two equal groups; tadalafil group received oral tadalafil (2 mg/kg/day), and PBS group received sterile PBS solution (normal saline; 2 mg/kg/day) for 28 days after the surgery. The right carotid arteries of all rabbits were anastomosed in an end-to-end fashion using 8/0 polypropylene suture. The rabbits were sacrificed at the end of the postoperative period of 28 days. After sacrificing, firstly anastomosis segment on the right carotid artery and secondly a part of the left carotid artery (as control) of each rabbit were removed. Morphometric examination of tissue sections was performed under a light microscope connected to an image capture system. RESULTS: There was a significant difference between the right and left carotid arteries in terms of intimal area and intima/media ratio both in tadalafil and PBS groups (p <0.001 for each). Intimal area and intima/media ratio were increased in the right carotid arteries compared to the left carotid arteries (p <0.001 for each). Besides, when the right carotid arteries of both groups were compared using covariance analysis, it was observed that intimal area and intima/media ratio in the anastomosis site were significantly reduced with tadalafil treatment (p <0.001). CONCLUSION: The present study was promising in terms of tadalafil use as a new agent for the prevention of neointimal hyperplasia, which is the leading cause of late-term graft failure in vascular surgery.

Ceftriaxone ameliorates cyclosporine A-induced oxidative nephrotoxicity in rat.

A growing body of evidence now suggested that cyclosporine A (CycA)-induced nephrotoxicity is a crucial clinical problem and oxidative stress is importantly responsible for its toxicity. Ceftriaxone induced antioxidant effect in brain and neuronal tissues against oxidative damage although its antioxidant potential effect on kidney has not been clarified. The aim of this study was to evaluate whether ceftriaxone protects CycA-induced oxidative stress kidney injury in rats. Twenty-four rats were equally divided into four groups. First group was used as control. Ceftriaxone (200 mg/kg) and CycA (15 mg/kg) were administrated to second and third groups for 10 days, respectively. The ceftriaxone and CycA combination was given to rats constituting the fourth group for 10 days. Lipid peroxidation (LP), urea nitrogen and lactate dehydrogenase (LDH) levels were higher in CycA group than in control and ceftriaxone groups although LP, urea nitrogen and LDH levels were lower in ceftriaxone + CycA group than in control and ceftriaxone groups. Glutathione peroxidase and catalase activities were lower in CycA group than in control whereas their activities were increased in control and ceftriaxone groups. Superoxide dismutase activity did not change by the treatments. Ceftriaxone administration recovered also CycA-induced atrophy, vacuolization and exfoliations of tubular epithelium and glomerular collapse in histopathological evaluation of kidney. In conclusion, we observed that ceftriaxone is beneficial on CycA-induced oxidative stress in kidney of rats by modulating oxidative and antioxidant system.

Dual effects of erdosteine on hemostasis via its different metabolites in young rats.

AIM: In the study, we examined erdosteine's effects on platelet functions and coagulation. MATERIALS AND METHODS: A total 29 young albino Wistar rats were divided into four groups. Control rats (n = 6) were given saline; Group 1 rats (n = 7) were given 3 mg/kg erdosteine by oral gavage for 3 days; Group 2 rats (n = 7) were given 10 mg/kg erdosteine by oral gavage for 3 days; and Group 3 rats (n = 9) were given 30 mg/kg erdosteine for 3 days. Twenty-four hours after the final dose, blood samples were drawn from a portal vein. Prothrombin time (PT), activated partial thromboplastin time (aPTT) and international normalized ratio (INR) were measured, and platelet counts were examined in a peripheral blood smear by light microscopy. RESULTS: PT and INR values of Group 1 increased compared to the controls but did not change in Group 3. Hemostatic parameters were not measured in Group 2 because the blood samples in Group 2's tubes clotted rapidly. Platelet counts of the peripheral blood from Group 2 were low but were normal in other groups. CONCLUSION: We have concluded erdosteine may disrupt hemostasis parameters by its different metabolites in patients. Erdosteine has dual effects on hemostasis via its different metabolites, which occur in different doses.

Salt and nitric oxide inhibition induced hypertension: the role of prostacycline and 8-isoprostane.

Renal prostacycline (PGI(2)) and oxidative stress are known to be important factors that effect the natriurezis and diuresis. 8-iso prostaglandin F(2)α± (8-isoprostane), a member of F(2)-isoprostanes, is formed from the nonenzymatic reaction of arachidonic acid and oxygen radicals in vivo and in vitro, and also it is a marker of oxidative stress in vivo. The aim of this study is to determine the role of renal PGI(2) and 8-isoprostane in a salt and nitric oxide (NO) inhibition-induced hypertension model. Rats were distributed equally among four groups (n = 6 per group). Control rats were given normal salt diet (0.32%); high-salt (HS) rats were given high salt diet (3.2%); NG-nitro-L-arginine (L-NNA) rats were given normal salt diet and 25 mg/kg L-NNA; HS+L-NNA rats were given high salt diet and 25 mg/kg L-NNA. Rats were placed in individual metabolic cages for 17 days. Systolic blood pressure (SBP) was measured at days initial, 7th and 14th .Urinary 8-isoprostane and PGI(2) levels were analyzed. Salt- loading alone did not change SBP values. The average SBP in L-NNA and HS+L-NNA groups were shown to significantly enhance compared to initial and day 7th in the same groups, respectively. The levels of 8-isoprostane in the HS+L-NNA group was significantly enhanced compared to the other groups. L-NNA or HS diet alone did not change the levels of 8-isoprostane compared to the control group. L-NNA alone did not change PGI(2) levels in urine compared to the control. PGI(2) levels in the HS, and the HS+L-NNA group was significantly higher compared to the control group. This study concluded that NOS inhibition plus salt-loading induced oxidative stress and increased renal PGI(2). Also, it is suggested that augmented oxidative stress may aggravate the hypertension. But the renal synthesis of PGI(2) is increased in order to augment the diuresis and natriuresis without the effect of blood pressure (BP).

Protective effects of thymoquinone against methotrexate-induced testicular injury.

Thymoquinone is the major active component derived from Nigella sativa. Methotrexate is a folic acid antagonist widely used in clinic. Aim of this study was to investigate the possible protective role of thymoquinone on testicular toxicity of methotrexate. Experiments were performed on male C57BL/6 mice (6 weeks old, 20 ± 2 g). The animals were divided into four groups with six mice in each group. Equivalent volumes of saline were injected intraperitoneally (i.p.) in the control group. In the thymoquinone group, mice received thymoquinone i.p. with a dose of 10 mg/kg/day for 4 days. Mice in the methotrexate group received single dose of methotrexate i.p., with a dose of 20 mg/kg. Finally, in the methotrexate plus thymoquinone group, in the first and the following 3 days after methotrexate administration, thymoquinone was injected with a dose of 10 mg/kg/day, i.p. At the end of the experiment, the left testis was quickly removed and divided into two parts for histological examination and biochemical analysis. Methotrexate alone increased total antioxidant capacity and myeloperoxidase activity compared to the controls. Thymoquinone treatment decreased total antioxidant capacity and prevented the increase in the myeloperoxidase activity. Light microscopy showed in mice that receiving methotrexate resulted in interstitial space dilatation, edema, severe disruption of the seminiferous epithelium and reduced diameter of the seminiferous tubules. Administration of thymoquinone reversed histological changes of methotrexate significantly. We suggest that thymoquinone use may decrease the destructive effects of methotrexate on testicular tissue of patients using this agent.

Letrozole induces hepatotoxicity without causing oxidative stress: the protective effect of melatonin.

AIM: The aim of this study was to determine the effects of letrozole (LTZ), an aromatase inhibitor (AI), and melatonin (MLT) on hepatic function and oxidative stress in female rats. MATERIAL AND METHODS: A total of 32 female rats were divided equally into four groups (n = 8). Control group received saline (0.5 ml/day, oral gavage). LTZ was administered to rats by daily oral gavage at 1 mg/kg dose. LTZ + MLT group was given LTZ (1 mg/kg, oral gavage) plus MLT (0.5 mg/kg/day, s.c.). MLT group was given MLT (0.5 mg/kg/day) by s.c. injection. The activities of superoxide dismutase (SOD) and catalase (CAT) and malondialdehyde (MDA) levels were measured in liver tissue. Total antioxidant capacity (TAC), total oxidant status (TOS), ALT, AST, GGT, ALP, LDH, bilirubin, BUN, creatinine, total cholesterol (TC), high-density lipoprotein (HDL) and triglyceride (TG) were assayed in serum samples. RESULTS: The oxidative stress parameters did not differ between groups. LTZ administration increased hepatic function parameters such as AST, LDH, ALP, bilirubin and MLT improved the disturbances of hepatic function. LTZ caused minimal histological changes in liver tissue and MLT treatment reversed those dejenerations. DISCUSSION: LTZ may cause hepatotoxicity without inducing oxidative stress and MLT restores hepatic activity.

The beneficial effects of tadalafil on renal ischemia-reperfusion injury in rats.

Acute renal failure due to ischemia-reperfusion (I/R) injury is a common complication in cardiovascular surgery. We determined the influence of tadalafil on renal injury in a renal I/R model in rats. For this purpose, 21 male Wistar albino rats were separated into 3 groups: sham, placebo and tadalafil. A right nephrectomy was performed, and the left renal pedicles were occluded for 60 min and reperfused for 60 min in the placebo and tadalafil groups. A single dose of tadalafil (10 mg/kg) through an orogastric tube was administered to the tadalafil group. Tubular atrophy with acute inflammation in renal histology, total oxidant status (TOS) and total antioxidant status (TAS) were determined in tissue homogenates. Compared to the tadalafil group, tubular atrophy and acute inflammation was significant in the placebo group. TAS levels were significantly higher in the tadalafil group compared to the placebo (p = 0.01) and sham groups (p = 0.04). While TOS levels were significantly higher in the placebo group (p = 0.03), tadalafil did not significantly alter the TOS levels. The beneficial effects of tadalafil can be attributed to its protective effects on renal tubular cells and inhibition of leukocyte infiltration in renal tissue. We think that tadalafil treatment has an important role in reducing renal injury resulting from renal I/R.

High plasma nesfatin-1 level in patients with major depressive disorder.

AIM: In the present study, our aim was to determine the changes in the plasma concentrations of a recently discovered peptide hormone nesfatin-1 in patients with major depressive disorder and then to make a comparison with the control group. METHOD: Subjects in the patient group were randomly selected from Mustafa Kemal University, Medical School, Research and Training Hospital, Psychiatry Department, Outpatient Clinic and subjects in the control group were selected from healthy volunteers. Healthy control subjects were matched in terms of weight and body mass index. Hamilton Depression Rating Scale (HAM-D) was applied to both groups. ELISA method was used for measurement of plasma nesfatin-1 levels. RESULTS: The average nesfatin-1 level was statistically higher in patients with major depressive disorder than in the control group (p<0.001). A positive correlation was observed between plasma nesfatin-1 levels and HAM-D scores both in the patient group (r=0.59, p<0.001) and in the control group (r=0.58, p<0.001). CONCLUSION: Our findings suggest a possible relationship between major depressive disorder and high plasma nesfatin-1 level.

Salt and nitric oxide synthase inhibition-induced hypertension: kidney dysfunction and brain anti-oxidant capacity.

The specific aim of this study was to examine the effects of salt-loading on kidney function and brain antioxidant capacity. Wistar rats were divided into four groups: Control rats were given normal drinking water and no drug treatment for 2 weeks. LNNA group: rats were given normal drinking water and the nitric oxide (NO) inhibitor NG-nitro-L-arginine (L-NNA), 3 mg/kg/day. LNNA + Salt group: rats were given drinking water containing salt 2% and 3 mg/kg L-NNA. Salt group: rats were given drinking water containing salt 2% and no drug treatment. Basal blood pressure and the levels of serum BUN, creatinine, uric acid, cortisol, electrolyte, serum antioxidant capacity, and oxidative stress were measured. NO, superoxide dismutase (SOD), and catalase (CAT) levels were measured in the hypothalamus, brainstem, and cerebellum. Salt overload increased the blood pressure of the LNNA + Salt group. Salt-loading enhanced BUN, creatinine, sodium retention. High salt produced an increase in uric acid levels and a decrease in cortisol levels in serum. Additionally, the oxidative stress index in serum increased in the LNNA + Salt group. Salt-loading enhanced brain NO levels, but not SOD and CAT activity. L-NNA increased brain SOD activity, but not CAT and NO levels. In conclusion, salt-loading causes hypertension, kidney dysfunction, and enhances oxidative stress in salt-sensitive rats.

Effects of caffeic acid phenethyl ester on isoproterenol-induced myocardial infarction in rats.

OBJECTIVE: Caffeic acid phenethyl ester (CAPE) is a natural product with potent anti-inflammatory, antitumor and antioxidant activities and attenuates inflammation and lipid peroxidation induced by ischemia-reperfusion injury. The purpose of the present study was to investigate the effects of CAPE on isoproterenol (ISO) -induced myocardial infarction. METHODS: A randomized controlled experimental design was used in this study. Rats were divided into four groups and treated with saline, CAPE, ISO and ISO+CAPE. Rats were treated with CAPE (10 micromol kg/day i.p.) or saline starting 3 days before injecting ISO (150 mg /kg s.c., 24 hours). Seven days later, rats were sacrificed and the hearts were excised for biochemical analyses and microscopic examination. One-way ANOVA test with post hoc multiple comparisons using LSD method were used for statistical analysis of the data. RESULTS: The administration of ISO alone resulted in higher myeloperoxidase (MPO) activity, lipid peroxidation, superoxide dismutase (SOD) and catalase (CAT) than in the control. The enzyme activities did not change in rat given CAPE alone. CAPE treatment prevented the increase in MPO activity and malondialdehyde, but did not affect the activities SOD and CAT enzymes. CONCLUSION: In light of these results, we conclude that CAPE prevents MPO-and lipid peroxidation-mediated myocardial injury via inhibition of neutrophil's MPO activity.

Protective effect of thymoquinone in experimental testicular torsion.

OBJECTIVES: To investigate the protective role of thymoquinone (TQ) on unilateral testicular ischemia-reperfusion (I/R) injury in mice. MATERIALS AND METHODS: Experiments were performed on male C57BL/6 mice (8 weeks old, 20-25 g). The animals were divided into 3 groups including 6 mice in each group: control (sham), torsion/detorsion (TD) and TD+TQ. Mice, except the sham-operated group, were subjected to left unilateral torsion (720° rotation in the clockwise direction). The experiments were finished after sham operation time for controls, 120 min torsion and 240 min detorsion for the other groups. In the TD+TQ group 10 mg TQ was injected intraperitoneally 30 min before detorsion. RESULTS: In the TD group total oxidative stress (TOS), oxidative stress index (OSI) and malondialdehyde (MDA) levels were higher than in the controls. TQ treatment decreased MDA, TOS and OSI values, but did not affect the total antioxidant capacity and myeloperoxidase activity in the TD+TQ group. Upon histological examination, mice in the TD group displayed moderate-to-severe disruption of the seminiferous epithelium. Treatment with TQ resulted in significantly reduced histological damage associated with I/R injury. CONCLUSION: Our results suggested that TQ treatment may have a protective effect on testicular I/R injury.

Effect of sulfite on antioxidant enzymes and lipid peroxidation in normal and sulfite oxidase-deficient rat erythrocytes.

Sulfite and related chemical such as sulfite salts and sulfur dioxide has been used as a preservative in food and drugs. This molecule has also been generated from the catabolism of sulfur-containing amino acids. Sulfite is a very reactive and potentially toxic molecule and has to be detoxified by the enzyme sulfite oxidase (SOX). The aim of this study was to investigate the effects of ingested sulfite on erythrocyte antioxidant status by measuring glucose-6-phosphate dehydrogenase (G-6-PD), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities and oxidant status by measuring thiobarbituric acid reactive substances (TBARS) in normal and SOX-deficient rats. Rats were assigned to four groups (n = 10 rats/group) as follows; control (C), sulfite (CS), deficient (D), and deficient + sulfite (DS). SOX deficiency was established by feeding rats a low molybdenum diet and adding to their drinking water 200 ppm tungsten (W). Sulfite (25 mg/kg) was administered to the animals via their drinking water. At the end of 6 weeks, Erythrocyte G-6-PD, SOD, and GPx but not CAT activities were found to be significantly increased with and without sulfite treatment in SOX-deficient groups. Sulfite treatment alone was also significantly increased erythrocytes' SOD activity in CS group compared to control. TBARS levels were found to be significantly increased in CS and DS groups and decreased in D group. When SOX-deficient rats treated with sulfite, TBARS level was still higher than other groups. In conclusion, these results suggested that erythrocyte antioxidant capacity, a defense mechanism against the oxidative challenge, increased by endogenous and exogenous sulfite due to its oxidant nature. This increase was also observed in CS and DS groups but it was insufficient to prevent lipid peroxidation.

Beneficial effect of erdosteine on methotrexate-induced testicular toxicity in mice.

Methotrexate is used to treat certain types of cancer of the breast, skin, head and neck, or lung. Methotrexate can cause serious or life-threatening side effects on liver, lungs, kidneys, and immune system. Methotrexate chemotherapy causes testicular damage in humans. The aim of this study was to investigate the possible protective role of erdosteine on testicular toxicity of methotrexate in mice. Twenty-six male mice were divided into four groups as follows: group 1, control; group 2, erdosteine-treated; group 3, methotrexate-treated; and group 4, methotrexate + erdosteine treated. On the first day of experiment, a single dose of methotrexate was intraperitoneally administered to groups 3 and 4, although a daily single dose of erdosteine was orally administered to group 2 and 4 for 7 days. At the end of the experiment, the testes of the animals were removed and weighed. The levels of total antioxidant capacity and total oxidative stress, and myeloperoxidase activity in the methotrexate group were higher than the control group (p<0.05). Lipid peroxidation levels were not changed in methotrexate group compared with control group. In conclusion, erdosteine could effectively protect the testes in methotrexate-induced toxicity.

Amitriptyline and tianeptine poisoning treated by naloxone.

INTRODUCTION: Severe amitriptyline toxicity may cause cardiac dysrhythmias, severe hypotension, convulsions and CNS depression, including coma. Management with gastric lavage, activated charcoal, alkalinization and supportive care with mechanical ventilation, antiarrhythmics and anticonvulsants, if required, is the general approach. CASE REPORT: A 33-year-old woman who had taken overdose antidepressants (amitriptyline and tianeptine) was admitted to the emergency service. She was intubated because she had pure respiratory arrest. Besides hypotension (80/60 mmHg), she was unresponsive to verbal and painful stimuli and her Glasgow coma score was 6. Hemogram and serum biochemical parameters and electrocardiography were within normal limits. The patient was examined for substance dependence and no trace of the injector was found in the body. Patient underwent a coma cocktail (naloxone 2 mg/body, 50% dextrose 25g/body and thiamin 100 mg/body). [corrected] Activated charcoal and intravenous alkalinization by NaHCO(3) were initiated. Spontaneous respiration started again 20 min after being given the coma cocktail. She became responsive to verbal stimuli first hour after the coma cocktail, and her Glasgow coma score improved to 13. She had spent 2 days in the service and was discharged by the second day of admission, without any complications. DISCUSSION: Herein, we report successful treatment in a case of severe amitriptyline and tianeptine poisoning by naloxone in addition to the above supportive care. Naloxone treatment may have a beneficial role in lethal doses of amitriptyline ingestion because amitriptyline may affect opioid receptors.

Prazosin treatment in the management of scorpion envenomation.

Scorpion stings represent an important and serious public health problem worldwide due to their high incidence and potentially severe and often fatal clinical manifestations. Children are at greater risk of developing severe cardiac, respiratory, and neurological complications due to lesser body surface area. Alpha receptor stimulation plays important role in the pathogenesis of pulmonary edema. Prazosin, a post synaptic alpha blocker, can be recommended as an effective drug in the treatment of serious scorpion envenomations with significant sympathetic symptoms. Oral prazosin is fast acting, easily available, relatively cheap, free from any anaphylaxis and highly effective.