Impact of caffeic acid phenethyl ester treatment on vancomycin-induced pancreatic damage in rats.

This study investigates the preventive effect of caffeic acid phenethyl ester (CAPE) on pancreatic damage induced by vancomycin (VCM) in rats. Rats were equally divided into three groups: group I (control), group II (only VCM-treated group) and group III (VCM + CAPE-treated groups). VCM was intraperitoneally administered at a dose of 200 mg kg(-1)twice daily for 7 days. CAPE was administered orally at 10 µM mL(-1) kg(-1) dose once daily for 7 days. The first dose of CAPE administration was performed 24 h prior to VCM injection. Blood and pancreas tissue samples were removed and collected after the study. Serum alkaline phosphatase (ALP), amylase, γ-glutamyl transferase (GGT) and lipase activities were determined. Pancreas tissue samples were evaluated with the light microscope. Group II significantly increased serum ALP, amylase, GGT and lipase activities when compared with the control group. Group III significantly decreased serum ALP, amylase, GGT and lipase activities when compared with group II. In histopathological examination, it has been observed that there was a significant pancreatic damage in group II. CAPE exerted prominent structural protection against VCM-induced pancreatic damage and this effect was statistically significant. CAPE caused a marked reduction in the extent of pancreatic damage. We have concluded that it may play an important role in the VCM-induced pancreatic damage and reduce the pancreatic damage both at the biochemical and histopathological aspects.

Factors affecting mortality in patients with organophosphate poisoning.

OBJECTIVE: To investigate the relationship between clinical and demographic characteristics and mortality in patients with organophosphate poisoning. METHODS: The retrospective study was conducted at Dicle University,Diyarbakir,Turkey, and comprised data of patients who presented with organophosphate poisoning between April 2004 and April 2013. The records were assessed in two groups, with Group 1 having data related to recovery, and Group 2 having data related to mortality. SPSS 16 was used for statistical analysis. RESULTS: Of the 296 patients, 219(74%) were women. Mortality was the outcome in 41(13.9%) cases. In Group 2, mean age, marital status, rural origin, presence of psychiatric disease, being illiterate, presence of nicotinic symptoms, and late admission were significantly higher than Group 1 (p<0.05 each). Logistic regression analysis indicated bradycardia as the most prominent independent predictor of mortality (p<0.001). Other independent predictors were age, glucose level, lactate dehydrogenase, coma and acidosis (p<0.05 each). CONCLUSIONS: Independent predictors of mortality in patients with organophosphate poisoning as bradycardia, age, glucose, lactate dehydrogenase level and acidosis.

Evaluation of the vasoplegic impact of papaverine in the rat aorta.

OBJECTIVE: To identify the degree of vasoplegic affinity of papaverine to rat thoracic aortas following constriction caused by adrenalin, serotonin and potassium chloride in an in-vitro model. METHODS: The in vitro vasoplegic efficacy of papaverine against adrenalin (10(-5) M), serotonin (5HT) (10(-4) M), and KCI (60 mM) was assessed, using a rat aortic vasospasm model in an organ bath. First, aortic rings were constricted with a submaximal dose of vasoconstrictor agents. The samples were then incubated with papaverine (3 x 10(-4) M) for 20 minutes, followed by readministration of the same vasoconstrictor agents. The first vasospastic response (before papaverine incubation) and the new vasoconstrictor responses (after papaverine incubation) of the vessels were then compared. RESULTS: The vasoplegic effect of vasoconstrictor agents in decreasing order was observed as adrenalin > KCl > 5HT. This different affinity for the vasoplegic effect is considered to be a temporary impact of the drugs and the maximal inhibition of vasoconstriction was detected for the adrenalin receptor. CONCLUSION: The relevance of the macromolecules is responsible for the permanent efficacy of the drugs. Different degrees of vasoconstriction were also obtained after papaverine administration, which suggests that different responses can occur as a result of different stimulation of receptor modulators.

The protective role of caffeic acid phenethyl ester against streptomycin ototoxicity.

OBJECTIVE: The aim of this experimental study was to investigate the efficacy of caffeic acid phenethyl ester (CAPE) in the prevention of streptomycin-induced ototoxicity. MATERIALS AND METHODS: Thirty-two adult Wistar albino rats were divided into 4 groups: control (n = 8), streptomycin (n = 8), CAPE (n = 8), and streptomycin + CAPE (n = 8). Rats were tested with distortion product otoacoustic emissions (DPOAEs) before drug administration. The animals in all groups were killed under general anesthesia on the 45th day following last DPOAE measurements. Hearing results were analyzed statistically to determine differences in amplitudes of DPOAE. Also, the cochleas of each rat were evaluated by histopathological and immunohistochemical examination. RESULTS: Significant difference was not observed in cochlear hair cells in the control and CAPE groups. In the streptomycin group, severe degeneration of hair cells and increased apoptotic cells were observed. In the streptomycin + CAPE group, although some deteriorations were observed, hair cells were mostly preserved. The DPgram of the streptomycin and streptomycin + CAPE groups was significantly deteriorated (P < .05). The analysis of the DPgram results revealed statistically significant differences between the groups of streptomycin and streptomycin + CAPE (P < .05). CONCLUSIONS: Caffeic acid phenethyl ester treatment attenuated hair cells injury in the inner ear, possibly via its antioxidant effect. Prophylactic administration of CAPE for streptomycin ototoxicity ameliorated hearing deterioration in rats.

The effects of caffeic acid phenethyl ester in acute methanol toxicity on rat retina and optic nerve.

PURPOSE: We aimed to test caffeic acid phenethyl ester (CAPE) as an antidote for acute methanol (MeOH) toxicity and to compare it with ethanol. METHODS: This study included five groups, each containing eight rats. The groups were control, methotrexate (MTX), MeOH, ethanol and CAPE. All rats except control group were treated with intraperitoneal (i.p.) MTX (0.3 mg/kg/d) for 7 d. At the 8th day of the experiment, i.p. injection of MeOH (3 g/kg) was administered in MeOH, ethanol and CAPE groups. Four hours after MeOH treatment, 0.5 g/kg ethanol was injected i.p. in ethanol group; 10 µmol/kg CAPE i.p. in CAPE group; serum physiologic i.p. in other groups. After 8 h, rats were anaesthetized and sacrificed. Total anti-oxidant status (TAS), total oxidant status (TOS) were measured on the dissected and excised retina and optic nerve samples. Fellow eyes were used for histopathologic evaluation and the cell count of retinal ganglion cell (RGC) layer. In addition, interactions of alcohol dehydrogenase with CAPE, ethanol, MeOH and pyrazole derivatives were investigated. RESULTS: Either CAPE or ethanol co-treatment decreased the TOS levels and increased the TAS levels compared to the MeOH group. MeOH treatment decreased the mean cell count in RGC layer. CAPE co-treatment significantly prevented cell loss (p = 0.040). Besides, in silico calculations showed that binding affinity of CAPE to alcohol dehydrogenase was higher than those of MeOH, ethanol, and pyrazole derivatives were. CONCLUSION: This study demonstrated that CAPE treatment decreased the oxidative stress in acute MeOH intoxication in the retina and optic nerve; beside that, protected RGC layer histology. In silico, CAPE had higher affinity score than MeOH, ethanol, pyrazole and pyrazole derivatives in the case of interaction with alcohol dehydrogenase.

The protective effects of caffeic acid phenethyl ester in isoniazid and ethambutol-induced ocular toxicity of rats.

PURPOSE: This study intended to examine the effect of caffeic acid phenethyl ester (CAPE) on isoniazid (INH) and/or ethambutol (ETM)-induced retina and optic nerve toxicity in a rat model. METHODS: This study included eight groups, each containing 10 rats. The groups were Control, INH, ETM, CAPE, INH+CAPE, ETM+CAPE, INH+ETM and INH+ETM+CAPE. Rats were given orally 50 mg/kg/d of INH and 50 mg/kg/d of ETM in tap water for 30 d. 10 µmol/kg of CAPE were intraperitoneally injected for 30 d. The first dose of CAPE was given 24 h before the INH and ETM treatment and continued until sacrifice. Control group was given only tap water for 30 d. Rats were anaesthetized and sacrificed on the 30th day of experiment. Superoxide dismutase (SOD) activities, malondialdehyde (MDA), total anti-oxidant status (TAS), total oxidant status (TOS) were measured on the dissected and excised retina and optic nerve samples. Fellow eyes were used for histopathologic evaluation and the retinal ganglion cell (RGC) count. In addition, CAPE, INH and ETM interaction with SOD isoforms were calculated in silico. RESULTS: The SOD activity and TAS levels were found significantly higher in CAPE-treated groups compared to INH and/or ETM-treated groups (p < 0.0001). But the MDA, and TOS levels were significantly lower in CAPE-treated groups (p < 0.0001). The mean RGC count is significantly decreased in INH, ETM and INH+ETM groups compared with INH+CAPE, ETM+CAPE and INH+ETM+CAPE groups, respectively (p values 0.001, 0.042, and 0.001 respectively). Besides, in silico calculations showed that binding affinity of CAPE to SOD isotypes was higher than that of INH and ETM. CONCLUSION: This study demonstrates that CAPE treatment may decrease the oxidative stress in the retina and optic nerve of INH- and ETM-treated rats and may prevent RGC loss. As an underlying mechanism, CAPE and SOD interaction seems crucial for alleviation of ocular oxidative stress and RGCs toxicity.

Histopathologic results of long-term sildenafil administration on rat inner ear.

OBJECTIVES: Sildenafil, a selective inhibitor of phosphodiesterase type 5, is widely used for the treatment of erectile dysfunction. Although cochlear effects of phosphodiesterase type 5 inhibitors remain still unclear because of inadequate data, some evidence that recently emerged indicates that these medications may be responsible for hearing impairment. In the present study, we aimed to examine the histopathologic effects of long-term sildenafil use on the cochlea in a rat model. METHODS: The study was performed with adult male Wistar albino rats. The control group was fed on standard laboratory diet. The study group was applied orally with sildenafil therapy, 1.5 mg/kg once a day for 45 days. Rats were anesthetized and decapitated. Each temporal bone was dissected, and the cochleas were removed en bloc. The inner-ear biopsy specimens were examined histologically with hematoxylin and eosin and caspase 3 immunoreaction under light microscopy. RESULTS: Hematoxylin and eosin staining showed no distinctive difference between the control group and the sildenafil group. With immunohistochemical examination, caspase 3 immunoreactivity was observed in the sildenafil group. In the control group, caspase 3 immunoreactivity was not observed. CONCLUSIONS: The caspase 3 immunoreactivity in the sildenafil group was strongly associated with an increase in apoptotic events in the cochlea. Long-term use of sildenafil can cause hearing impairment through increased apoptosis.

The effect of cadmium toxicity on renal nitric oxide synthase isoenzymes.

The aim of this study was to assess the cadmium (Cd) toxicity on renal nitric oxide synthase (NOS) isoenzymes. The study was carried out on 18 inbred male (Cd group: 10 and control group: 8) Wistar rats. Cd group received drinking water containing 15 mg/L Cd for 30 days; and at the end of the 30 days, plasma Cd was analysed. One kidney was snap frozen to assess the endothelial NOS (eNOS), inducible NOS (iNOS) and neuronal NOS (nNOS) expressions by Western blot analyses, and the other kidney was preserved for histopathological examination. Plasma Cd levels were significantly elevated in the Cd group. The Western blot analyses found higher levels of eNOS, iNOS and nNOS in the Cd group but only eNOS and nNOS levels were statistically significant. There was no difference in pathological assessment of the renal tissues. Cd toxicity increases NOS isoenzyme levels and may affect renal physiology.

Mild hypoglycaemic attacks induced by sulphonylureas related to CYP2C9, CYP2C19 and CYP2C8 polymorphisms in routine clinical setting.

AIM: To evaluate the impact of polymorphisms in the cytochrome P450 (CYP) 2C9, 2C19 and 2C8 genes on the risk of mild hypoglycaemic attacks in patients treated with sulphonylureas. METHODS: One hundred and eight type 2 diabetic patients (50 men, 58 women), treated with oral antidiabetics, including at least one from the sulphonylurea group (glimepiride n = 50, gliclazide n = 46, or glipizide n = 12) for 3 months or longer, were included in the study. Symptoms of hypoglycaemia (sweating, tremor, anxiety and palpitations) during a 3 month period were recorded and confirmed by home glucose measurements. Gender, age, body mass index, creatinine clearance, HbA1c, oral antidiabetic dose and concomitant medication were assessed together with functional CYP2C9, CYP2C19 and CYP2C8 polymorphisms, analysed by real-time PCR methods. RESULTS: Fifteen patients (eight men, seven women) reported hypoglycaemia symptoms which were validated by their home glucose measurements (< 70 mg/dl). Heterozygosity and homozygosity for CYP2C9 variant alleles (*2 or *3) tended to be more frequent among patients who reported hypoglycaemic attacks (60 and 7%) than those who did not (39 and 3%). Similarly, the CYP2C8*1/*3 genotype tended to be more frequent in patients with (47%) than without (27%) hypoglycaemia, while no such trend was observed for CYP2C19 variants. However, only in the gliclazide group a significant association between CYP2C9 genotype and hypoglycaemic attacks was observed (P = 0.035). None of the other covariates showed any significant association with the risk of hypoglycaemic attacks. CONCLUSIONS: CYP2C9 polymorphisms leading to decreased enzyme activity show a modest impact on the risk of mild hypoglycaemia attacks during oral antidiabetic treatment, with a significant association in patients treated with gliclazide.

Routine enzymes in the monitoring of type 2 diabetes mellitus.

We examined the relationships of glucose and HbA1c levels with the routinely screened serum enzyme activities in type 2 diabetes mellitus, and we designed an in vitro study to evaluate the direct effect of glucose levels on enzyme activities. The study was performed on a consecutive series of outpatients with type 2 diabetes who were followed up at Dicle University Medical Faculty Hospital from May 2009 to May 2010 for the first time. Effects of aspartate transaminase, aminotransferase, gamma-glutamyl transferase (GGT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) activities, glucose and HbA1c levels and in vitro glucose (492, 287, 184, 131, 82 mg dl⁻¹, respectively) on enzymes were determined. The patients were categorized on the basis of glucose and HbA1c levels and grouped according to a range of values. In patients with high HbA1c levels (>10.1%), ALP, GGT activities and creatine kinase (CK)-MB/CK (p = 0.008, 0.026, 0.014) ratio were increased significantly when compared with those in the control group. In patients with high glucose levels (> 200 mg dl⁻¹), ALP, GGT activities and CK-MB/CK ratio (p = 0.003, 0.001, 0.001) were increased significantly when compared with those in the control group. Glucose, which was added to serum in different concentrations in vitro, did not directly affect enzyme activities such as ALP, GGT and CK. We concluded that increased glucose levels could damage the liver and the heart muscle cells. Monitoring of blood glucose levels is a more valuable parameter than monitoring HbA1c in the momentary evaluation of diabetes.

The protective effect of erdosteine on vancomycin-induced pancreatic damage in rats.

OBJECTIVE: The goal of this study was to investigate whether vancomycin (VCM) has a negative effect on pancreatic tissue and to elucidate the role of erdosteine (ERD), an expectorant and an antioxidant agent, on possible VCM-induced pancreas impairment in rats. MATERIALS AND METHODS: A total of 21 male Wistar albino rats were included in this study. All animals were equally divided into three groups as follows: Controls (n = 7), VCM treated group (200 mg/kg twice daily for 7 days intraperitoneally, n = 7) and VCM (200 mg/kg) + ERD treated group (10 mg/kg day orally ERD, n = 7). The first dose of ERD administration was performed 24 h prior to VCM injection and the study was continued for 7 days. At the end of the study, all animals were sacrificed. Blood and pancreas tissue samples were collected. For biochemical analysis, serum amylase, lipase, alkaline phosphatase (ALP), and gamma glutamyl transferase (GGT) activities were measured. For histopathological examination, pancreas tissue samples were investigated under the light microscope. RESULTS: VCM administration has significantly increased the serum amylase, lipase, ALP, and GGT activities, when compared with the controls. VCM + ERD administration significantly decreased the serum lipase, amylase, and GGT activities. There was no statistically significant difference between the VCM + ERD treated group and only VCM treated group by means of serum ALP levels. It has been observed that there was a prominent pancreatic tissue damage in only VCM given group. However, ERD exhibited structural protection against VCM-induced pancreatic damage and this effect was statistically significant. ERD has also obtained a marked reduction in the extent of pancreatic damage. CONCLUSION: Erdosteine may play an important role in the VCM-induced pancreatic damage and may reduce the pancreatic damage both in biochemical and histopathological aspects.

Influence of electromagnetic fields on bone fracture in rats: role of CAPE.

OBJECTIVE: To study the effects of radiation emitted by mobile phones on bone strength and caffeic acid phenethyl ester (CAPE) on the changes induced by radiation. METHODS: Forty-eight Sprague-Dawley rats were divided into five groups. Rats in the control group (first group) were left within the experimental setup for 30 min/day for 28 days without radiation exposure. Nine hundred MHz radiation group was broke down into 2 subgroups (group 1/2). Both subgroups were exposed to radiation for 28 days (30 min/day). The next group was also divided into 2 subgroups (group 3/4). Each was exposed to 1800 MHz of radiation for 28 days (30 min/day). The third and fifth groups were also treated with CAPE for 28 days. Treatment groups received ip caffeic acid phenethyl ester (10 micromol/kg per day) before radiation session. Bone fracture was analyzed. RESULTS: Breaking force, bending strength, and total fracture energy decreased in the irradiated groups but increased in the treatment groups. CONCLUSION: Radiation and CAPE can significantly improve bone.

Caffeic acid phenethyl ester prevents cadmium-induced cardiac impairment in rat.

Caffeic acid phenethyl ester (CAPE), a flavonoid like compound, is one of the major components of honeybee propolis. It was found to be a potent free radical scavenger and antioxidant recently. The aim of this study was to examine the effect of CAPE on cadmium (Cd)-induced hypertension and cardiomyopathy in rats. In particular, nitric oxide (NO) may contribute to the pathophysiology of Cd induced cardiac impairment. Malondialdehyde (MDA, an index of lipid peroxidation) levels and nitric oxide (NO, a vasodilator) levels were used as markers Cd-induced cardiac impairment and the success of CAPE treatment. Also, the findings have been supported by the histopathologic evidences. The rats were randomly divided into three experimental groups each (12), as follows: the control group, Cd-treated group (Cd) and Cd plus CAPE-treated group (Cd+CAPE). CdCl(2) in 0.9% NaCl was administrated intraperitoneally (i.p.) with a dose of 1mg/kg/day. CAPE was co-administered i.p. a dose of 10 microM/kg for 15 days. Hypertension was found to be induced by intraperitoneal administration of Cd in a dose of 1mg/kg/day on the measurements taken 15 days later. MDA levels were increased (p<0.001) in cardiac tissue and NO levels were decreased (p<0.05) in serum in the Cd group than those of the control group had. On the other hand, there was a slight difference (increase) in MDA levels in the Cd+CAPE group than the ones in the control group (p<0.003). In addition, MDA levels were decreased and NO levels were increased in the Cd+CAPE group compared with the Cd group (p<0.001, p<0.0001, respectively). As a result, treatment with CAPE significantly reversed the increased lipid peroxidation (LPO) product, MDA, and decreased NO levels in Cd treated animals. In the histopathologic examination, a significant hypertrophy in atrial and ventricular myofibrils was observed in only Cd administered group, in comparison with the control group. There was no statistically significant difference between the CAPE given and control groups by means of atrial and ventricular myofibril diameters. In conclusion, the underlying mechanism of the myocardial hypertrophy may be related to hypertension due to inhibition of NO production in the vessels, and CAPE has a protective effect on Cd-induced hypertension mediated cardiac impairment in the rats.

Effects of magnesium sulfate on airway smooth muscle contraction in rats.

Aim To investigate the effect of magnesium sulfate (MgSO4) at different doses on isolated tracheal smooth muscle contraction in rats induced by different mechanisms. Methods Twelve rats' tracheas were placed into organ bath. Consecutively, acetylcholine (10-6,10-5,10-4 M), histamine(10-8,10-5,10-3 M) and KCl (30,60 mM) solutions was administered for contractions. MgSO4 from 10-4 to 10-1 M concentrations were subsequently administered after each constrictive agent and relaxation degrees were recorded. Results In the acetylcholine and KCl groups, dose dependent strong contractions were observed, but not in the histamine group and that group was excluded. Significant relaxation occurred with gradually increasing doses of MgSO4. In the high dose KCl group, a slight increase in contractions after the administration of 10-4 and 10-3 M MgSO4 was recorded. Conclusion We suggest that MgSO4 is effective in relaxing airway smooth muscle contractions caused by different factors; however, it must be considered that low doses of MgSO4 may only lead to a slight increase in contractions.

Nitric oxide level in the nasal and sinus mucosa after exposure to electromagnetic field.

OBJECTIVE: The purpose of this study was to examine the changes in nitric oxide (NO) level in the nasal and paranasal sinus mucosa after exposure radiofrequency electromagnetic fields (EMF). STUDY DESIGN AND SETTING: Thirty male Sprague-Dawley rats were randomly grouped as follows: EMF group (group I; n, 10), EMF group in which melatonin received (group II; n, 10) and the control (sham operated) group (group III; n, 10). Groups I and II were exposed to a 900 MHz. Oral melatonin was given in group II. Control rats (group III) were also placed in the tube as the exposure groups, but without exposure to EMF. At the end of 2 weeks, the rats were sacrificed, and the nasal and paranasal sinus mucosa dissected. NO was measured in nasal and paranasal mucosa. RESULTS: The nasal and paranasal sinus mucosa NO levels of group I were significantly higher than those of the control group (group III) ( P < 0.05). However, there was no statistically significant difference between group II and the control group (group III) regarding NO output ( P > 0.05). CONCLUSION: Exposure to EMF released by mobile phones (900 MHz) increase NO levels in the sinus and nasal mucosa. SIGNIFICANCE: Increased NO levels may act as a defense mechanism and presumably related to tissue damage. In addition, melatonin may have beneficial effect to prevent these changes in the mucosa.

Effects of short-term hyperglycemia on the vasoconstriction of the aorta.

BACKGROUND/AIM: To investigate vasoconstrictor responses of healthy blood vessels to short-term hyperglycemic conditions such as postprandial hyperglycemia, gestational diabetes mellitus, and steroid-induced diabetes. MATERIALS AND METHODS: Female Wistar rat aorta rings were incubated in normal (11 mM) and high (22 mM and 44 mM) glucose concentrations for 4 h. Responses of vasoconstriction were measured in reaction to serotonin (10-5 M), phenylephrine (10-6 M), and KC1 (60 mM) compared to the ambient condition, including different glucose concentrations. RESULTS: While the responses of vasoconstriction to KC1 were increased in the presence of Krebs' solution with high glucose, no statistically significant changes were observed in the reaction to serotonin and phenylephrine. In addition, malondialdehyde levels were increased in hyperglycemic conditions. CONCLUSION: Short-term hyperglycemia may lead to augmented contractile response in aorta rings through several mechanisms, and our results showed that oxidative stress is probably one of them.

Protective role of caffeic acid phenethyl ester on serum cholinesterase inhibition by acute exposure to diazinon in rats.

AIM: To evaluate whether caffeic acid phenethyl ester (CAPE), a flavonoid-like natural compound plentifully found in beeswax, has a protective effect on diazinon-induced serum cholinesterase (ChE) inhibition in rats. MATERIALS AND METHODS: Animals were divided into 4 groups. The first animal group was not treated with any substance. The second animal group was orally given a 200 mg/kg body weight (bw) sublethal dose of diazinon. The third animal group was injected intraperitoneally with 2.84 mg (10 micromol)/kg bw of CAPE 1 day prior to administration of 200 mg/kg bw of diazinon orally. The fourth animal group was intraperitoneally injected with 2.84 mg (10 tmol)/kg bw of CAPE 30 min after 200 mg/kg bw of diazinon was orally administered. RESULTS: Analysis of the animal blood samples obtained 48 h after diazinon administration revealed that diazinon decreased serum ChE activity by 75%, while CAPE administration 24 h prior to and 30 min following diazinon application improved serum ChE activity by 25%-32% as compared to levels with diazinon administration only. In silico studies suggest that CAPE prevents diazinon from binding to butyryl ChE due to a higher binding affinity than that of diazinon. CONCLUSION: Our laboratory findings suggest that CAPE plays a protective role against butyryl ChE inhibition by diazinon.

Magnesium and diltiazem relaxes phenylephrine-precontracted rat aortic rings.

Perioperative vasospasm during cardiovascular surgery is a challenging problem. Several vasodilator agents are frequently utilized for its prevention in surgical practice. Magnesium and diltiazem both have known potential vasorelaxant effects. We planned to compare the efficacy of diltiazem and magnesium in relieving phenylephrine-precontracted rat aortic rings. Ten young adult female Wistar albino rats weighing 230-260 g were used in this study. The aortic rings in the organ bath equilibrated and reached their baseline tension. Precontraction was induced by 0.001 mmol/l phenylephrine and cumulative concentration-relaxation curves were obtained by consecutively increasing the addition of either diltiazem (10(-6)-0.1 mmol/l) or magnesium (0.1-10 mmol/l). The mean maximal relaxation responses observed by diltiazem and magnesium on separate aortic rings were 90 ± 3 and 53 ± 2%, respectively. The calculated EC50 of diltiazem was 0.01035 mmol/l, whereas the EC50 of magnesium was 4.064 mmol/l (P < 0.05). Both magnesium and diltiazem produced vasorelaxation on phenylephrine-precontracted rat aortic rings in this study, but the potency of diltiazem regarding the EC50 value was significantly higher than that of magnesium. Magnesium could be a candidate together with diltiazem to inhibit vasospasm on arterial grafts during coronary bypass surgery.

Relationships between respiratory function disorders and serum copper levels in copper mineworkers.

The aim of this study was to investigate the respiratory function disorders that could be related to dust exposure during the production of copper mine in copper mineworkers (CMWs). The study included 75 male CMWs (mean age, 32.0 ± 7.1 years, 58.6% smokers) and 75 male age- and smoking status-matched healthy control subjects. Serum Cu level was significantly higher in the CMW group (0.80 ± 0.62 µg/ml) than the control group (0.60 ± 0.39 µg/ml) (p = 0.017). Significant negative correlations were found between serum Cu level and forced expiratory volume in first second (r = -0.600; p < 0.001) and between serum Cu level and forced vital capacity (r = -0.593; p = <0.001) in CMWs. Serum Cu level was significantly higher in the restrictive type pulmonary function disorders group (1.36 ± 0.62 µg/ml) than obstructive type (0.90 ± 0.55 µg/ml) and normal pulmonary function pattern group (0.53 ± 0.43 µg/ml) (p < 0.001). Patients with radiological parenchymal abnormalities had significantly higher serum copper levels than those without abnormalities (1.53 ± 0.52 vs. 0.71 ± 0.52 µg/ml, respectively; p = 0.002). In conclusion, result of the study has shown a negative association between pulmonary functions disorders and radiological abnormalities and serum Cu levels in CMWs.

Increased caspase-3 immunoreactivity of erythrocytes in STZ diabetic rats.

Eryptosis is a term to define apoptosis of erythrocytes. Oxidative stress and hyperglycemia, both of which exist in the diabetic intravascular environment, can trigger eryptosis of erythrocytes. In this experimental study, it is presented that the majority of erythrocytes shows caspase-3 immunoreactivity in streptozocin- (STZ)-induced diabetic rats. Besides that, caspase-3 positive erythrocytes are aggregated and attached to vascular endothelium. In conclusion, these results may start a debate that eryptosis could have a role in the diabetic complications.