bluuebunny/crossref_metadata_2025_split huggingface dataset:
Coenzyme Q10‐containing composition (Immugen®) protects against occupational and environmental stress in workers of the gas and oil industry
Authors: Korkina Ludmila , Deeva Irina , Ibragimova Galina , Shakula Alexander , Luci Antonio , Luca Chiara De 
Published: December 2008

AbstractThe manual workers of the gas‐and‐oil extraction industry are exposed to hostile environmental and occupational conditions, resulting in elevated mortality and disability, due to chronic neurological and cardiovascular diseases. We evaluated the degree of oxidative stress, often associated with these pathological features, in the blood of manual and office employees of Russian Siberian extraction plants, and their psycho‐physiological conditions. Results showed increased levels of spontaneous (p < 0.05) and PMA‐activated (p < 0.01) luminol‐dependent chemiluminescence (LDCL) in the white blood cells (WBC), and decreased peroxynitrite levels (p < 0.05) in the group of manual workers, and less markedly in the clerks and technicians working on spot, vs. a control group of city clerks. Superoxide release by WBC, and plasma/WBC membrane ubiquinol levels did not display major differences in the three groups. A relevant percentage of manual/office workers of extraction platforms presented impaired cardiovascular and neurological functions. The short term administration of a nutraceutical formulation based on coenzyme10, vitamin E, selenium, methionine and phospholipids led to significant improvement of cardiovascular parameters and psycho‐emotional status, consistent with the normalization of LDCL and peroxynitrite production by WBC, with a good compliance to treatment confirmed by the increased blood levels of ubiquinol.
The effect of Cyclosporine A chronic administration on the antioxidant pattern of rat liver mitochondria: Structural and functional consequences
Authors: Battino Maurizio , Bompadre Stefano , Leone Luciana , Pugnaloni Armanda , Rubini Corrado , Ferreiro Maria Soledad , Gallardo Isabel , Bullon Pedro 
Published: December 2008

AbstractCyclosporine A (CsA) plays a pivotal role in controlling Ca2+movement in the cell modulating also the mitochondrial permeability transition pore. We investigated if chronic administration of CsA may have some effects on the lipophilic and hydrophilic antioxidant pattern of rat liver mitochondria and on their morphological structure. It seems that CsA administration does not statistically affect the redox status of the antioxidants investigated and their amounts (vitamin E, CoQ9, CoQ10, glutathione,uric acid and ascorbic acid) despite the variety of effects that this treatment produces at physiological and morphological levels. However, some kind of derangement could occur in the liver biochemical machinery since CsA treatment induces a markedly increased variability in antioxidant contents.
The effects of Coenzyme Q10 on locomotor and behavioral activity in young and aged C57BL/6 mice
Authors: Sinatra Drew S. , Sinatra Stephen T. , Heyser Charles J. 
Published: December 2008

AbstractTo explore the possibility that Coenzyme Q10 (CoQ10) supplementation stabilizes psychomotor behavioral function in the aging organism, the behavioral effects of CoQ10 were evaluated in young adult male C57BL/6 mice (3 months of age) and aged C57BL/6 mice (24 months of age). Mice treated with CoQ10 exhibited significantly greater locomotor activity as reflected by an increase in square crosses than non‐drug controls. The administration of CoQ10 increased all aspects of exploratory behavior in the open field. The effect was uniform across all mice and did not interact with age.Younger animals and aged animals treated with CoQ10 may adapt rapidly to novel areas, or they are less fearful of exploration. The behavioral activation observed in CoQ10 treated mice may be the result of increased locomotor activity, psychomotor stimulation, or decreased anxiety.
Coenzyme Q10, antioxidant status and ApoE isoforms
Authors: Battino M. , Giunta S. , Galeazzi L. , Galeazzi R. , Mosca F. , Santolini C. , Principi F. , Ferretti G. , Bacchetti T. , Bencivenga R. , Piani M. , Riganello G. , Littarru G. P. 
Published: December 2008

AbstractThe aim of this study was to inquire the antioxidant status in plasma and lipoproteins isolated from normal subjects possessing different ApoE genotypes. For this purpose we investigated blood samples from 106 healthy blood donors: the distribution of ApoE alleles (E2/E2 = 0.9%, E2/E3 = 10.4%, E2/E4 = 2.8%, E3/E3 = 71.7%, E3/E4 = 12.3% and E4/E4 1.9% with 1, 11, 3, 76, 13, and 2 subjects respectively for each genotype) was in agreement with previous data. Almost no differences were found in the concentrations of both coenzyme Q10 (CoQ10) and vitamin E for the different genotypes. Concentration of CoQ10 in isolated lipoproteins was also similar, in the different genotypes, when referred to cholesterol; CoQ10 in LDL was higher for the E3/E3 subjects when referred to protein. Neither CoQ10 nor vitamin E correlated with paraoxonase (PON) activity or cholesteryl‐ester hydroperoxides (CHP). Furthermore, there was no correlation between the same lipophilic antioxidants and CHP levels. The only E2 homozygous subject found had high levels of PON and low levels of CHP; the two E4/E4 subjects had low PON activity together with low levels of CHP.
Peroxiredoxins in antioxidant defense and redox regulation
Authors: Flohé Leopold , Budde Heike , Hofmann Birgit 
Published: December 2008

AbstractPeroxiredoxins constitute a family of peroxidases that lack prosthetic groups or catalytically active heteroatoms. Instead, their peroxidatic activity is due to a strictly conserved cysteine that is activated within a novel catalytic triad in which the cysteine thiol is coordinated to an arginine and a threonine or serine residue. Donor substrates are thiol compounds which differ between subtypes of peroxiredoxins and species. In pathogenic trypanosomatids that lack heme‐ or seleno‐peroxidases peroxiredoxins have been shown to represent the major devices to detoxify hydroperoxides and an equivalent role may be assumed for other protozoal parasites and many bacterial pathogens. In mammals equipped with more efficient peroxidases the peroxiredoxins appear to be responsible for the redox regulation of diverse metabolic processes. The substantial differences in the cosubstrate requirements of the peroxiredoxins of pathogenic microorganisms and their mammalian host may be exploited to selectively inhibit the antioxidant defense of pathogens. Thereby, the pathogen would be more readily eliminated by the innate immune response of the host's phagocytes.
Oxidative stress: The special case of diabetes
Authors: Wiernsperger N. F. 
Published: December 2008

AbstractThe implication of oxidative stress (OS) in diabetes is a major concern for the development of therapeutics aimed at improving the metabolic and/or vascular dysfunctions of this burdening disease. Ample evidence is available suggesting that OS is present in essentially all tissues and can even be observed in prediabetic states. This raises the question of the origin of OS and suggests that, although hyperglycemia is largely linked with free radical production, its role may mainly be the aggravation of a preexisting state. Indeed other factors are also causally linked to OS, such as hormones and lipids. The main debate is about the pertinence of antioxidant therapy since the large scale clinical trials performed recently have essentially failed to show any significant improvement in metabolic or vascular disturbances of diabetic patients. However this conclusion must be tempered by the fact that they have mainly been using vitamin E +/‐C; indeed many arguments suggest that either the choice or the application modalities of these substances may have been inadequate. Potential reasons for the actual failure of antioxidant therapy in diabetes are discussed; the indisputable involvement of OS in this disease still leaves hope for alternative therapeutic approaches.
Time‐dependent enhancement in mitochondrial glutathione status and ATP generation capacity by schisandrin B treatment decreases the susceptibility of rat hearts to ischemia‐reperfusion injury
Authors: Chiu Po Yee , Ko Kam Ming 
Published: December 2008

AbstractIn the present study, we examined the time‐dependent changes in the mitochondrial glutathione status and ATP generation capacity in the myocardium as well as the susceptibility of the myocardium to ischemia‐reperfusion (IR) injury in female Sprague Dawley rats treated with a single pharmacological dose (1.2 mmol/kg) of schisandrin B (Sch B). Sch B treatment produced a time‐dependent enhancement in myocardial mitochondrial glutathione status, as evidenced by increases in myocardial mitochondrial reduced glutathione (GSH) level and activities of glutathione reductase, Se‐glutathione peroxidase (GPX) and glutathione S‐transferases, with the response reaching maximum at 48 h post‐dosing and then declining gradually to the control level at 96 h post‐dosing. The enhancement of mitochondrial glutathione status was associated with an increase in myocardial ATP generation capacity, with the value peaking at 72 h post‐dosing. These beneficial effects of Sch B on the myocardium was paralleled by a time‐dependent decrease in the susceptibility to IR injury, with the maximum protection demonstrable at 48 h post‐dosing. The cardioprotection was associated with increases in myocardial GSH level and activities of glutathione antioxidant enzymes (except for GPX whose activity was suppressed) as well as tissue ATP level/ATP generation capacity. The results suggest that Sch B treatment can precondition the myocardium by enhancing the mitochondrial glutathione status and ATP generation capacity, thereby protecting against IR injury.
Iron status and oxidative stress in β‐thalassemia patients in Jakarta
Authors: Laksmitawati D. R. , Handayani S. , Udyaningsih‐Freisleben S. K. , Kurniati V. , Adhiyanto C. , Hidayat J. , Kusnandar S. , Dillon H. S. D. , Munthe B. G. , Wirawan R. , Soegianto R. R. , Ramelan W. , Freisleben H. J. 
Published: December 2008

AbstractA study on thalassemia intermedia and major patients in Jakarta was initiated to obtain a comprehensive picture of metabolic dysregulation, iron overload, oxidative stress, and cell damage. Data are presented from a group of 14 transfusion‐dependent patients in an age range of 11‐25 years (T) and another group of 9 frequently transfused (for at least 15 years) patients aged 17‐30 years (L). A third group comprised 6 patients (aged 7 to 14 years) who had not yet obtained transfusions (N). The 21 controls (C) were voluntary students without diagnosis or clinical signs of thalassemia up to 30 years of age. The study was approved by the Ethical Clearance Board of the Medical Faculty and all blood samples from controls and patients were obtained on fully informed consent. Levels of antioxidants (vitamins A, C, E and β‐carotene) and reactive thiols are considerably decreased in transfused patients, whereas signs of iron overload and cell damage are increased (serum iron, ferritin, transferrin saturation, SGOT, SGPT, γ‐GT, bilirubin). Results can be summarized that non‐transfused thalassemia intermedia patients exert slight signs of oxidative stress, and increased hemoglobin degradation but no significant indication of tissue or cell damage. This picture differs considerably from transfusion‐dependent thalassemia major patients: highly significant decrease in antioxidants and thiols and tremendous iron overload and cell damage. The picture is even worsened in long‐term transfused patients. Iron chelation after transfusion is not sufficient in Indonesia, because it is normally (with few exceptions) applied only once together with transfusion. Hence, one major reason of the bad condition of transfusion‐dependent thalassemia patients in Indonesia appears to be frequent transfusions (on the average one per month) and insufficient chelation of one treatment per month together with transfusion.
Molecular mechanisms of cholesterol or homocysteine effect in the development of atherosclerosis: Role of vitamin E
Authors: Özer Nesrin Kartal , Negis Yesim , Aytan Nurgul 
Published: December 2008

AbstractThe development of atherosclerosis is a multifactorial process in which both elevated plasma cholesterol levels and proliferation of smooth muscle cells play a central role. Numerous studies have suggested the involvement of oxidative processes in the pathogenesis of atherosclerosis and especially of oxidized low density lipoprotein. Some epidemiological studies have shown an association between high dietary intake and high serum concentrations of vitamin E and lower rates of ischemic heart disease. Cell culture studies have shown that α‐tocopherol brings about inhibition of smooth muscle cell proliferation. This takes place {via} inhibition of protein kinase C activity. α‐Tocopherol also inhibits low density lipoprotein induced smooth muscle cell proliferation and protein kinase C activity. The following animal studies showed that vitamin E protects development of cholesterol induced atherosclerosis by inhibiting protein kinase C activity in smooth muscle cells in vivo.Elevated plasma levels of homocysteine have been identified as an important and independent risk factor for cerebral, coronary and peripheral atherosclerosis. However the mechanisms by which homocysteine promotes atherosclerotic plaque formation are not clearly defined. Earlier reports have been suggested that homocysteine exert its effect via H2O2 produced during its metabolism. To evaluate the contribution of homocysteine in the pathogenesis of vascular diseases, we examined whether the homocysteine effect on vascular smooth muscle cell growth is mediated by H2O2. We show that homocysteine induces DNA synthesis and proliferation of vascular smooth muscle cells in the presence of peroxide scavenging enzyme, catalase. Our data suggest that homocysteine induces smooth muscle cell growth through the activation of an H202 independent pathway and accelerate the progression of atherosclerosis.The results indicate a cellular mechanism for the atherogenicity of cholesterol or homocysteine and protective role of vitamin E in the development of atherosclerosis.
Isolated erythrocyte membranes of transfusion‐dependent and non‐transfused thalassemia patients in Jakarta, investigated by electron paramagnetic resonance spectroscopy
Authors: Udyaningsih‐Freisleben Seruni K. , Kurniati Vita , Prasetyo Pamulih B. , Handayani Sri , Adhiyanto Chris , Soegianto Rondang R. , Pudiantari Ratna , Munthe Bulan G. , Ramelan Wahyuning , Freisleben Hans‐Joachim 
Published: December 2008

AbstractErythrocyte membrane structural parameters were studied in transfusion‐dependent β‐thalassemia patients, in long‐term transfused patients (regularly transfused < 15 years), and in those who had not yet obtained transfusions. Controls were voluntary students up to 30 years of age without diagnosis or clinical signs of thalassemia. Membranes were isolated and investigated by sodium dodecylsulfate polyacrylamide gel electrophoresis (SDS‐PAGE) and electron paramagnetic resonance (EPR) spectroscopy. Data obtained from the thiol‐reactive spin label N‐ethyl‐maleimidoproxyl reveal immobilization of protein environment in erythrocyte membranes from thalassemic patients. SDS‐PAGE shows both degradation and aggregation of membrane proteins. Thalassemic erythrocyte membranes exert higher order parameters in the hydrophobic region as determined by 16‐doxyl‐stearic acid. Rotational correlation times of this spin label increase only in transfused patients. Polarity is higher in membranes of all patients than in controls. In the polar interface, order parameters obtained from 5‐doxyl‐stearic acid increase in non‐transfused and decrease in transfusion‐dependent patients as compared with controls. Transfused patients exert increasing membrane order in the hydrophobic region and counter‐currently decreasing order in the polar interface indicating loss of membrane integrity along with the loss of fluidity and polarity gradients and the loss the energetic barrier function of the membrane.
Thiocyanate overload and thyroid disease
Authors: Erdoǧan Murat Faik 
Published: December 2008

AbstractThiocyanate [SCN−] is a complex anion which is a potent inhibitor of iodide transport. It is the detoxification product of cyanide and can easily be measured in body fluids. Consumption of naturally occurring goitrogens, certain environmental toxins and cigarette smoke can significantly increase SCN− concentrations to levels potentially capable of affecting the thyroid gland. Goiter endemics were reported to develop when the critical urinary iodine/ SCN− ratio decreases below 3 μg iodine per mg SCN−. Iodine supplementation completely reverses the goitrogenic influence of SCN−. SCN− is also generated from cigarette smoking as a detoxifying product of cyanide. During the past two decades many reports dealt with the possible effects of cigarette smoking on thyroid hormone synthesis, thyroid gland size and thyroid autoimmunity including infiltrative ophtalmopathy of Graves' disease. In this mini‐review, issues regarding thiocyanate overload and thyroid disease will be summarized.
Flavonoids and thyroid disease
Authors: Van Der Heide Daan , Kastelijn Jan , Schröder‐Van Der Elst Janny P. 
Published: December 2008

AbstractThe most potent natural plant‐derived compounds that can affect thyroid function, thyroid hormone secretion and availability to tissues is the group of flavonoids, i.e. plant pigments. They are present in our daily food, such as vegetables, fruits, grains, nuts, wine, and tea. Epidemiological studies suggest beneficial effects on health of flavonoids, which are commonly attributed to their activity as antioxidants. Experimental studiesin vitro, however, showed inhibition of organification in thyroid cells and follicles by several flavonoids. Studiesin vivoandvitrowith synthetic and natural flavonoids showed displacement of T4from transthyretin leading to disturbances in thyroid hormone availability in tissues. Radioactive labeled flavonoids appeared to be eliminated rapidly from the body mainly through excretion in the feces. In pregnant rats synthetic flavonoids cross the placenta and accumulate in the fetal compartment, including the fetal brain. Therefore, a high intake of flavonoids is contraindicated. In conclusion: flavonoids show strong interference with many aspects of thyroid hormone synthesis and availability.
Role of iodine in antioxidant defence in thyroid and breast disease
Authors: Smyth Peter P.A. 
Published: December 2008

AbstractThe role played in thyroid hormonogenesis by iodide oxidation to iodine (organification) is well established. Iodine deficiency may produce conditions of oxidative stress with high TSH producing a level of H2O2, which because of lack of iodide is not being used to form thyroid hormones. The cytotoxic actions of excess iodide in thyroid cells may depend on the formation of free radicals and can be attributed to both necrotic and apoptotic mechanisms with necrosis predominating in goiter development and apoptosis during iodide induced involution. These cytotoxic effects appear to depend on the status of antioxidative enzymes and may only be evident in conditions of selenium deficiency where the activity of selenium containing antioxidative enzymes is impaired. Less compelling evidence exists of a role for iodide as an antioxidant in the breast. However the Japanese experience may indicate a protective effect against breast cancer for an iodine rich seaweed containing diet. Similarly thyroid autoimmunity may also be associated with improved prognosis. Whether this phenomenon is breast specific and its possible relationship to iodine or selenium status awaits resolution.
Selenium and thyroid function in infants, children and adolescents
Authors: Chanoine Jean‐Pierre 
Published: December 2008

AbstractSelenium is an integral component of the enzymes glutathione peroxidase (GPx) and iodothyronine deiodinases. Although selenium nutrition could conceivably affect thyroid function in infants, children and adolescents, available data suggest that the effect of selenium deficiency on thyroid function is relatively modest. In patients with isolated selenium deficiency (such as patients with phenylketonuria receiving a low‐protein diet), peripheral thyroid hormone metabolism is impaired but there are no changes in thyrotropin (TSH) or clinical signs of hypothyroidism, suggesting that these patients are euthyroid. Selenium supplementation may be advisable to optimize tissue GPx activity and prevent potential oxidative stress damage. In areas where combined selenium and iodine deficiencies are present (such as endemic goiter areas in Central Africa), selenium deficiency may be responsible for the destruction of the thyroid gland in myxoedematous cretins but may also play a protective role by mitigating fetal hypothyroidism. In these areas, selenium supplementation should only be advocated at the same time or after iodine supplementation. In patients with absent or decreased production of thyroid hormones and who rely solely on deiodination of exogenous L‐thyroxine for generation of the active triiodothyronine (such as patients with congenital hypothyroidism), selenium supplementation may optimize thyroid hormone feedback at the pituitary level and decrease stimulation of the residual thyroid tissue.
Oxidative stress and Graves' ophthalmopathy: In vitro studies and therapeutic implications
Authors: Bartalena Luigi , Tanda Maria Laura , Piantanida Eliana , Lai Adriana 
Published: December 2008

AbstractGraves' ophthalmopathy (GO) is a disorder of autoimmune origin caused by a complex interplay of endogenous and environmental factors. After recognition of one or more antigens shared by thyroid and orbit, activated T lymphocytes infiltrating the orbit trigger a cascade of events leading to production of cytokines, growth factors and oxygen reactive species. Proliferation of adipocytes and fibroblasts then follows, with an increased synthesis of glycosaminoglycans (GAG), which attract water and cause edema of orbital structures and venous congestion. Proliferation of orbital fibroblasts and adipocytes, both in the retroocular tissue and in the perimysium of extraocular muscles, are among the most important events leading to the increased volume of orbital structures (fibroadipose tissue and extraocular muscles). The contribution of oxygen reactive species to the changes occurring in the orbit is underscored by in vitro studies. Superoxide radical stimulates orbital fibroblasts to proliferate and to produce GAG. Furthermore, hydrogen peroxide induces expression of HLA‐DR and heat shock protein‐72, involved in antigen recognition and T‐lymphocyte recruitment. Cigarette smoking, which is probably the most important environmental factor associated with GO occurrence and maintenance, might also act, among other mechanisms, by enhancing generation of oxygen reactive species and reducing antioxidant production. Substances such as nicotinamide, allopurinol and pentoxifylline reduce superoxide‐ or hydrogen peroxide‐induced proliferation of fibroblasts, GAG production and HLA‐DR or HSP‐72 expression by GO orbital fibroblasts, possibly through scavenging oxygen free radicals. Two small, non‐randomized and/or uncontrolled studies investigated the effects of nicotinamide, allopurinol or pentoxifylline on GO. Favorable results were reported, but data are not fully convincing and the true effectiveness of these agents needs to be verified in randomized, controlled trials enrolling a larger number of patients.It currently seems unlikely that they may find a relevant place in the limited armamentarium available for the management of severe GO.