Effects of coenzyme Q10 on the heart ultrastructure and nitric oxide synthase during hyperthyroidism

Coenzyme Q10 is an important component of mitochondrial electron transport chain and antioxidant. Hyperthyroidism manifests hyperdynamic circulation with increased cardiac output, increased heart rate and decreased peripheral resistance. The heart is also under the oxidative stress in the hyperthyroidism. The aim of this study was to examine both how the coenzyme Q10 can affect heart ultrastructure in the hyperthyroidism and how the relationship between nitric oxide synthase (NOS) and heart damage and coenzyme Q10. Swiss Black C57 mice received 5 mg/kg L-thyroxine. Coenzyme Q10 (1.5 mg/kg) and L-thyroxine together was given to second group mice. Coenzyme Q10 and serum physiologic were applied to another two groups, respectively. All treatments were performed daily for 15 days by gavage. Free triiodothyronine and thyroxine were increased in two groups given L-thyroxine; thyroid-stimulating hormone level did not change. Hyperthyroid heart showed an increased endothelial NOS (eNOS) and inducible NOS (iNOS) immunoreactivity in the tissue. Coenzyme Q10 administration decreased these NOS immunoreactivities in the hyperthyroid animals. Cardiomyocytes of the hyperthyroid animals was characterized by abnormal shape and invaginated nuclei, and degenerative giant mitochondria. Desmosome plaques reduced in density. In hyperthyroid mice given coenzyme Q10, the structural disorganization and mitochondrial damage regressed. However, hearts of healthy mice given coenzyme Q10 displayed normal ultrastructure, except for increased mitochondria and some of them were partially damaged. Coenzyme Q10 increased the glycogen in the cardiomyocytes. In conclusion, coenzyme Q10 administration can prevent the ultrastructural disorganization and decrease the iNOS and eNOS increment in the hyperthyroid heart.     

Integration of Visual Information in Auditory Cortex Promotes Auditory Scene Analysis through Multisensory Binding

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The Corynebacterium glutamicum mycothiol peroxidase is a reactive oxygen species‐scavenging enzyme that shows promiscuity in thiol redox control

Cysteine glutathione peroxidases (CysGPxs) control oxidative stress levels by reducing hydroperoxides at the expense of cysteine thiol (‐SH) oxidation, and the recovery of their peroxidatic activity is generally accomplished by thioredoxin (Trx). Corynebacterium glutamicum mycothiol peroxidase (Mpx) is a member of the CysGPx family. We discovered that its recycling is controlled by both the Trx and the mycothiol (MSH) pathway. After H₂O₂ reduction, a sulfenic acid (‐SOH) is formed on the peroxidatic cysteine (Cys36), which then reacts with the resolving cysteine (Cys79), forming an intramolecular disulfide (S‐S), which is reduced by Trx. Alternatively, the sulfenic acid reacts with MSH and forms a mixed disulfide. Mycoredoxin 1 (Mrx1) reduces the mixed disulfide, in which Mrx1 acts in combination with MSH and mycothiol disulfide reductase as a biological relevant monothiol reducing system. Remarkably, Trx can also take over the role of Mrx1 and reduce the Mpx‐MSH mixed disulfide using a dithiol mechanism. Furthermore, Mpx is important for cellular survival under H₂O₂ stress, and its gene expression is clearly induced upon H₂O₂ challenge. These findings add a new dimension to the redox control and the functioning of CysGPxs in general.     

VACTERL-H associated with central hypothyroidism: a case report

The VACTERL-H syndrome is a rare combination of vertebral anomalies, anal atresia, congenital heart defects, tracheo-esophageal fistula, abnormalities of kidneys and limb anomalies together with hydrocephalus. This condition is recognized as a hereditary entity with poor prognosis. We present a newborn weighing 3400 g, born by cesarean section to a 27 years old mother who had had an irregular antenatal follow-up. The patient had severe hydrocephalus, proximal esophageal atresia and distal tracheoesophageal fistula, gastric outlet obstruction, imperforated anus and recto-urethral fistula, patent ductus arterious, a bifid scrotum, a vertebral defect, sacral dimple and central hypothyroidism. The patient had no limb defects. The association of central hypothyroidism and VACTERL-H has previously not been reported.     

Synthesis of dihydrochalcones of Myrica gale

4,4,6-Trimethyl-2-(3-phenylpropionyl)cyclohexane-1,3,5-trione, 2′-hydroxy-4′,6′-dimethoxy-3′-methyldihydrochalcone, 2′,6′-dihydroxy-4′-methoxy-3′,5′-dimethyldihydrochalcone and 2,2,5-trimethyl-4(3-phenylpropionyl)cyclopent-4-ene-1,3-dione, constituents of Myrica gale, have been synthesized.     

The effect of oxytocin and PGF2alpha on the uterine involution and pregnancy rates in postpartum Arabian mares

In this study, the effects of oxytocin and an analog of prostaglandin (cloprostenol) on the uterine involution and pregnancy rates were investigated. Mares received 3 ml of 0.9% NaCl in Group C (n=10), 30 IU/mare of oxytocin in Group O (n=10) and 250 microg/mare of cloprostenol in Group P (n=10) within 12h after parturition. The gravid uterine horn's cross-sectional diameter was measured by ultrasonography. The mean uterine diameters did not differ significantly between the treatment (O and P) and the control (C) groups (p>0.05). The difference between the postpartum ovulation periods (Group C: 12.6+/-0.72 days, Group O: 15+/-1.33 days, Group P: 14.6+/-1.11 days), the pregnancy rates at foal heat (Group C: 60%, Group O: 60%, Group P: 80%) and the embryonic death rates at foal heat (Group C: 33.3%, Group O: 16%, Group P: 25%) were not found to be statistically significant between the treatment and the control groups. The mean progesterone concentrations were similar in all groups and decreased continuously from parturition to until foal heat (Group C: from 2.43+/-0.24 to 0.66 ng/ml, Group O: from 3.07+/-0.6 to 0.27+/-0.27 ng/ml and Group P: from 2.8+/-0.44 to 0 ng/ml) (p>0.05). In conclusion, it was decided that the oxytocin and PGF2alpha treatments performed on the mares with the purpose of stimulating involution had no effect on the duration of parturition-first ovulation, the shrinkage of the uterus diameter, the pregnancy and embryonic death rates.     

Effects of atorvastatin therapy on hypercholesterolemic rabbits with respect to oxidative stress, nitric oxide pathway and homocysteine

Hypercholesterolemia is characterized with changes in lipid profile, nitric oxide pathway and oxidative stress markers. This study is designed to evaluate the effects of hypercholesterolemic diet and atorvastatin therapy on oxidative stress, lipid peroxide and thiobarbituric acid reactive substances (TBARS), NO pathway markers, nitric oxide(NO) and asymmetric dimethylarginine (ADMA), homocysteine, and paraoxonase activity (PON1) in rabbits. Twenty rabbits fed with high-cholesterol diet for 8 weeks were randomly divided into 2 groups on the fourth week of the hypercholesterolemic diet. First group was fed with high-cholesterol diet alone, whereas the second group with the same cholesterol diet plus atorvastatin (0.3 mg/kg/day) for 4 weeks. High-cholesterol diet increased total cholesterol, low density lipoprotein (LDL-C), high density lipoprotein (HDL-C), ADMA, TBARS and lipid peroxide levels and reduced PON1 activity and NO levels in rabbits. Four weeks of atorvastatin therapy significantly increased HDL-C, PON1 activity and reduced LDL-C, TBARS and lipid peroxide concentrations. Atorvastatin therapy is beneficial in decreasing oxidative stress related with hypercholesterolemia, mainly affecting lipid profile and PON1 activity.     

Donor heart preservation with iloprost supplemented St. Thomas Hospital cardioplegic solution in isolated rat hearts

This study was designed to assess the influence of St. Thomas Hospital cardioplegic solution (St. Th.) on heart preservation in rat hearts subjected to 6h ischemia when supplemented with iloprost. In the control group (n=8), nothing was added to St. Th., whereas 10 or 1000 nmol L(-1) iloprost was added in the second (n=7) and third (n=8) groups, respectively. Mechanical contraction parameters, cardiac tissue damage and oxidative stress markers were evaluated. The 10 nmol/L iloprost group peak systolic pressure (71.0+/-30.9 versus 41.0+/-9.4 mm Hg) and -dp/dtmax (1103.8+/-94.3 versus 678.6+/-156.8 mm Hg s(-1)) were significantly higher than control group at 30 min of reperfusion (p<0.05). Iloprost supplemented groups had higher GSH and catalase levels of coronary perfusate at reperfusion, in comparison with initial values (p<0.05). AST, CK, CK-MB values increased at 0 min of reperfusion and cTnI values at 45 min of reperfusion (p<0.05) in all groups with no difference between groups. According to our results, iloprost supplementation had mild but significant improvement in postischemic values in mechanical and oxidative stress parameters, resulting in better heart preservation.