Effect of smoking intensity on thyroid volume, thyroid nodularity and thyroid function: the Melen study.

AIM: The purpose of our study was to determine the association between smoking habit, goiter, thyroid functions and ultrasonographic nodularity in moderately iodine deficient area. METHODS: The MELEN study is a prospectively designed survey on the prevalence of thyroid diseases in Turkish adults. A total of 2298 subjects with a mean age of 50 (age range 18 to 92) were interviewed. Smoking habits were registered from questionnaires and subsequent interviews with a physician. Thyroid ultrasonography was performed and interpreted by the same experienced physician, using the same equipment. After an overnight fast, blood samples were collected from all the study subjects for the determination of serum free thyroxine, thyroid stimulating hormone (TSH) were measured. RESULTS: Mean thyroid volumes of current smokers were significantly lower than either former or never smokers (P=0.014). There were no difference according to smoking habits on goiter and established multinodularity in current smokers (P<0.05). Heavy smokers (>20 pack/year) had higher thyroid volumes, higher goiter and multinodular goiter (MNG) prevalence than moderate smokers (P<0.001). Thyrotoxicosis (TSH<0.35) cases were more frequent among heavy smokers than moderate smokers (14.1% versus 8.2%, P<0.001; respectively). Heavy smoking independently predicted goiter (odds ratio: 1.459 [95% confidence interval: 1.029 and 2.068]; P=0.034). CONCLUSION: Heavy smoking was associated with increased prevalence of thyroid multinodularity and goiter in respect to moderate smoking. No association was found between smoking habit and thyroid dysfunction.

A case of Seckel syndrome with Tetralogy of Fallot.

Seckel syndrome, also known as Harper's Syndrome and Virchow-Seckel-Syndrome, was first described by Seckel in 1960, and is a rare (<1:10,000 live births) autosomal recessive trait. The syndrome (OMIM 210600) is a form of primordial dwarfism, characterized by severe intrauterine growth restriction, postnatal dwarfism, severe microcephaly with variable mental retardation, facial anomalies and skeletal abnormalities. Cardiac anomalies have been described in only five case. We report a male newborn with typical findings of Seckel sydrome associated with Tetrology of Fallot. This is the first case reported in concomitance with Tetralogy of Fallot, and might be a new finding of the syndrome. We would like to emphasize that clinicians should perform diagnostic interventions for congenital cardiac defects in Seckel Syndrome.

Impairment of endothelium-dependent vasorelaxation in cadmium-hypertensive rats.

Abnormalities in the production and/or release of relaxing factors from the endothelium have been implicated in the development of hypertension in several animal models. Endothelium-dependent relaxation has been reported to be impaired in thoracic aorta in experimentally induced and genetically hypertensive rats. Present study has extented these observations to thoracic aorta of cadmium-hypertensive rats. The possible role of alterations in oxidant status was also studied. Hypertension was induced by the intraperitoneal administration of 1 mg/kg/day cadmium for 15 days. Mechanical responses produced by acetylcholine (ACh, 10(-9)-10(-4) M) and sodium nitroprusside (SNP, 10(-10)-10(-5) M) were studied on phenylephrine-precontracted thoracic aorta rings from control and cadmium-hypertensive rats. Serum nitric oxide (NO) and aortic malondialdehyde (MDA) levels were measured. ACh-induced relaxation was attenuated in aorta from cadmium-hypertensive rats, whereas relaxation responses to SNP did not differ significantly between the groups. Exposure of aortic rings to N(G)-nitro-L-arginine methyl ester (L-NAME, 10(-4) M) resulted in a significantly greater inhibition of relaxation response to ACh in aortic rings of cadmium-hypertensive rats as compared with control rats. Incubation with L-arginine (L-Arg, 10(-3) M) caused a similar reversal of the inhibition of ACh-induced relaxation by L-NAME in both groups. Serum NO levels were decreased and aortic MDA levels were increased in cadmium-treated rats as compared with control rats. However, the differences between the groups did not reach a statistical significance. These findings suggested that the reduction in endothelium-dependent relaxation may play a role in cadmium-induced hypertension as it was in many other hypertension models.

The effects of diazinon on lipid peroxidation and antioxidant enzymes in rat heart and ameliorating role of vitamin E and vitamin C.

Diazinon is one of the most widely used organophosphate insecticides (OPIs) in agriculture and public health programs. Reactive oxygen species (ROS) caused by OPIs may be involved in the toxicity of various pesticides. The aim of this study was to investigate how diazinon affects lipid peroxidation (LPO) and the antioxidant defense system in vivo and the possible ameliorating role of vitamins E and C. For this purpose, experiments were done to study the effects of DI on LPO and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in adult rat heart. Experimental groups were: (1) control group, (2) diazinon treated (DI) group, (3) DI+vitamins E and C-treated (DI+Vit) group. The levels of malondialdehyde (MDA) and the activities of SOD and CAT increased significantly in the DI group compared with the control group. The activity of SOD and the levels of MDA decreased significantly in the DI+Vit group compared with the DI group. The differences between the DI+Vit and control groups according to the MDA levels and the activities of both SOD and CAT were statistically significant. These results suggest that treating rats with a single dose of diazinon increases LPO and some antioxidant enzyme activities in the rat myocardium and, in addition, that single-dose treatment with a combination of vitamins E and C after the administration of diazinon can reduce LPO caused by diazinon, though this treatment was not sufficiently effective to reduce the values to those in control group.

The effects of subchronic methidathion toxicity on rat liver: role of antioxidant vitamins C and E.

Methidathion (MD) phosphorodithioic acid S-[(5-methoxy-2-oxo-1,3,4-thiadiazol-3(2H)-yl)methyl] O,O-dimethyl ester is the organophosphate insecticide (OPI) most commonly used worldwide in the pest control of crops. Subchronic MD exposure was evaluated for its effects on lipid peroxidation, the serum activities of cholinesterase (ChE), and enzymes concerning liver damage, and the protective effects of combination of vitamins E and C in albino rats. Additionally, the histopathological changes in liver tissue were examined. Experimental groups were as follows: control group; a group treated with 5 mg/kg body weight MD (MD group); and a group treated with 5 mg/kg body wight MD plus vitamin E plus vitamin C (MD+AO group). The MD and MD+AO groups were treated orally with MD on five days a week for 4 weeks. The serum activities of cholinesterase (ChE), alanine transferase (ALT), aspartate amiotransferase (AST), lactate dehydrogenase (LDH), gamma-glutamyltransferase (GGT), alkaline phosphatase (ALP), and the concentration of malondialdehyde (MDA) and liver histopathology were studied. In serum samples, MD significantly increased MDA concentration and ALP, AST, GGT, LDH activities but decreased the ALT and ChE activities. In the MD+AO group, MDA level and ALP, AST, LDH activities were significantly decreased and ChE activity was increased compared to the MD group. Histopathological changes found in liver tissue of rats treated with MD included were infiltration with mononuclear cells in all portal areas, sinusoidal dilatation, and focal microvesicular steatosis and hydropic degenerations in parenchymal tissue. The severity of these lesions was reduced by administration of vitamins. From these results, it can be concluded that subchronic MD causes liver damage, and lipid peroxidation may be a molecular mechanism involved in MD-induced toxicity. Furthermore, the combination of vitamins E and C can reduce the toxic effects of MD on liver tissue of rats.