bluuebunny/crossref_metadata_2025_split huggingface dataset:
Bioremediation of selenium‐contaminated sediments and water
Authors: Frankenberger William T. , Arshad Muhammad 
Published: December 2008

AbstractSelenium (Se) is a contaminant of agricultural irrigation‐drainage water in the western United States, and the cause of wildlife deaths and grotesque deformities. Some approaches in reducing the toxic Se concentrations from contaminated sediments and water have been proposed, but most of these tend to be costly or ineffective. Bioremediation through microbial transformations of toxic Se species into nontoxic forms is being considered as an effective remedial alternative. The microbial reduction of toxic oxyanions of Se {SeO42 and SeO32‐} into insoluble Se0 or methylation of these species to dimethylselenide (DMSe) has been accepted as a potential bioremediation strategy for cleanup of Se‐contaminated water and sediments. By conducting a series of laboratory, bench‐scale and field studies, we have thoroughly investigated the remedial potential of these approaches. It was observed that microorganisms, particularly Enterobacter cloacea, are very active in reduction of Se oxyanions present in irrigation drainage water, into insoluble Se0and, by monitoring various environmental conditions and addition of organic amendments, the process could be stimulated manifold. Similarly, the process of biomethylation of Se in soil sediments and water was found active and highly dependent on specific carbon amendments (pectin and proteins), pH, temperature, moisture, aeration and activators (cofactors). Moreover, Se biomethylation was protein/peptide‐limited rather than nitrogen‐, amino acid‐ or carbon‐limited. Crude casein and its components were equally stimulatory producing a > 50‐fold enhancement in DMSe yield. Methionine and methyl cobalamin stimulated DMSe production by Alternaria alternata, indicating that the coenzyme may mediate the transfer of a methyl group to the Se atom. An acute toxicity test involving inhalation of DMSe by rats revealed that DMSe is nontoxic. Experiments were scaled up from laboratory studies to field plots to verify the feasibility of this bioremediation approach. Based upon the promising results of these studies, a biotechnology prototype was developed which could be applicable for cleanup of polluted sediments and water throughout the western United States.
Removal of soluble selenium by a selenate‐reducing bacterium Bacillus sp. SF‐1
Authors: Kashiwa Masami , Ike Michihiko , Mihara Hisaaki , Esaki Nobuyoshi , Fujita Masanori 
Published: December 2008

AbstractIn order to develop a biological process for removal of selenium from industrial wastewater, Bacillus sp. strain SF‐1 was isolated from selenium‐contaminated sediment. The bacterium reduces selenate to selenite and subsequently to nontoxic insoluble elemental selenium using lactate as an electron donor and selenate as an electron acceptor in an anaerobic condition. Elemental selenium transformed from soluble selenium was deposited both inside and outside of the cells. Since the selenate reduction rate of the strain SF‐1 was higher than the selenite reduction rate, selenite was transiently accumulated. In an experiment of the repeated soluble selenium reduction by strain SF‐1, 0.5 mM of selenate was sequentially treatable with a cycle of one day. Thus, our sequential system for removal of soluble selenium is very useful.
Dietary copper and dimethylhydrazine affect protein kinase C isozyme protein and mRNA expression and the formation of aberrant crypts in colon of rats
Authors: Davis Cindy D. , Johnson W. Thomas 
Published: December 2008

AbstractLow dietary copper has been shown to decrease the expression of various protein kinase C (PKC) isozymes and increase the risk of colon cancer development in experimental animals. The purpose of this study was to investigate the relationship between dietary copper and carcinogen administration on PKC isozyme accumulation and aberrant crypt foci (ACF) formation in rats fed 0.9 and 7.7 μg Cu/g diet. After 24 and 31 d on the diets, the rats were injected with either dimethylhydrazine (DMH) (25 mg/kg i.p.) or saline and killed at two time points (2 wk and 8 wk after DMH). Rats fed low dietary copper had significantly lower (p<0.0001) hematocrits, hemoglobin, ceruloplasmin activity and plasma and liver copper concentrations than rats fed adequate dietary copper. Ingestion of low dietary copper significantly (p<0.005) increased the formation of DMH‐induced ACF (116.8 vs 59.6). Low dietary copper significantly (p<0.05) decreased the concentration of PKC α, δ, and ζ in the colon at 2 wk but not at 8 wk. Thus, changes in PKC isoform protein concentration may be related to increased susceptibility of copper‐deficient animals to colon cancer.
Biological effects of a nano red elemental selenium
Authors: Zhang Jin‐Song , Gao Xue‐Yun , Zhang Li‐De , Bao Yong‐Ping 
Published: December 2008

AbstractA novel selenium form, nano red elemental selenium (Nano‐Se) was prepared by adding bovine serum albumin to the redox system of selenite and glutathione. Nano‐Se has a 7‐fold lower acute toxicity than sodium selenite in mice (LD50 113 and 15 mg Se/kg body weight respectively). In Se‐deficient rat, both Nano‐Se and selenite can increase tissue selenium and GPx activity. The biological activities of Nano‐Se and selenite were compared in terms of cell proliferation, enzyme induction and protection against free racial‐mediated damage in human hepatoma HepG2 cells. Nano‐Se and selenite are similarly cell growth inhibited and stimulated synthesis of glutathione peroxidase (GPx), phospholipid hydroperoxide glutathione peroxidase (PHGPx) and thioredoxin reductase (TR). When HepG2 cells were co‐treated with selenium and glutathione, Nano‐Se showed less pro‐oxidative effects than selenite, as measured by cell growth. These results demonstrate that Nano‐Se has a similar bioavailability in the rat and antioxidant effects on cells.
Absorption and excretion of orally administered inositol hexaphosphate (IP6 or phytate) in humans
Authors: Grases Felix , Simonet Bartolomé M. , Vucenik Ivana , Prieto Rafel M. , Costa‐Bauzá Antonia , March Joan G. , Shamsuddin Abulkalam M. 
Published: December 2008

AbstractA study of the pharmacokinetic profile (oral absorption and renal excretion) of inositol hexaphosphate or phytate (IP6) is presented. Seven healthy volunteers were following a IP6 poor diet (IP6PD) in a first period, and on IP6 normal diet (IP6ND) in a second one. When following the IP6PD they become deficient in IP6, the basal levels found in plasma (0.07± 0.01 mg/L) being clearly lower than those found when IP6ND was consumed (0.26± 0.03 mg/L). During the restriction period the maximum concentration in plasma were obtained 4 h after the ingestion of a single dose of IP6, observing almost the same renal excretion profiles for the three different comercial sources and doses. After the IP6 restriction period, volunteers were on IP6ND, reaching normal plasma and urinary IP6 values in 16 days. Thus, the normal plasma and urinary concentrations, can be obtained either by comsumption of a IP6ND taking a long time or in a short period by IP6 supplements.
Transport of methotrexate into LNCaP human prostate cancer cells
Authors: Horne Donald W. , Reed Kathleen A. 
Published: December 2008

AbstractUptake of methotrexate into the LNCaP human prostate cancer cells was linear for the first 60∼min. The initial rate of methotrexate uptake was highest at extracellular pH 4.5 and decreased markedly until pH 7.0 to 8.0. Transport of methotrexate into LNCaP cells showed two components, one saturable ‐Km = 0.13 ± 0.06 μM and Vmax = 1.20 ± 0.16 pmol · 45 min−1 · mg−1 protein at low concentrations and the other apparently not saturable up to 10 μM. Uptake of methotrexate was inhibited by structural analogs with the Ki values being 6.53, 12.4, and 85.6 μM for 5‐formyltetrahydrofolate, 5‐methyltetrahydrofolate, and folic acid, respectively. Uptake of methotrexate into LNCaP cells was not inhibited by the energy poisons in contrast to methotrexate uptake into PC‐3 prostate cancer cells. Uptake was inhibited by increasing concentrations of sulfate and phosphate ions and by the organic anions probenecid and DIDS, suggesting that methotrexate may be transported by an anion‐exchange mechanism. These results show that methotrexate is transported into LNCaP prostate cancer cells by a carrier‐mediated process.
Antioxidant effects of α‐ and γ‐carboxyethyl‐6‐hydroxychromans
Authors: Yoshida Yasukazu , Niki Etsuo 
Published: December 2008

AbstractCarboxyethyl‐6‐hydroxychromans (CEHC), the major metabolites of both tocopherols (Toc) and tocotrienols (Toc‐3), have been found in human plasma. In the present study, the antioxidant properties of α‐ and γ‐CEHC were measured and compared with α‐ and γ‐ tocopherols. Following results were obtained: (1)α‐ and γ‐CEHC have the same reactivities toward radicals and exert the same antioxidant activities against lipid peroxidation in organic solution as the corresponding parent tocopherols respectively; (2) the partition coefficient decreased in the order α‐Toc (3.36) > γ‐Toc (3.14) > α‐CEHC (2.26) > pentamethyl‐6‐chromanol (1.92) > γ‐CEHC (1.83) > 0 > Trolox (‐0.97); (3) α‐ and γ‐CEHC scavenge aqueous radicals more efficiently but they inhibit the lipid peroxidation within the membranes less efficiently than the corresponding α‐ and γ‐Toc, respectively; (4) α‐CEHC inhibits the oxidation synergistically with ascorbate; and (5) α‐ andγ‐CEHC reduce Cu(II) to give Cu(I) and corresponding quinones as major product, but the prooxidant effect of CEHC in the presence of cupric ion was small. These results imply that CEHC may act as an antioxidant in vivo especially for those who take tocopherol supplement.
Detoxification of electrophilic compounds by glutathione S‐transferase catalysis: Determinants of individual response to chemical carcinogens and chemotherapeutic drugs?
Authors: Coles Brian F. , Kadlubar Fred F. 
Published: December 2008

AbstractThe glutathione S‐transferases (GSTs) catalyze the GSH‐dependent detoxification of reactive electrophiles such as genotoxic chemical carcinogens and cytotoxic chemotherapeutic agents. Allelic polymorphism in the GSTs has been used to investigate the hypothesis that GSTs are involved in susceptibility to human cancers. Such studies have resulted in low penetrance, high prevalence associations between cancer risk and GST polymorphisms. By examination of interindividual variation of GST expression it becomes clear that GST genotype alone is not an accurate predictor of GST expression. GST expression is tissue specific and interindividual variation of expression is at least 7‐fold in normal tissues. Thus, populations of the same genotype are actually heterogeneous as regards expression. Similarly, polymorphisms are not effective in all tissues and GST induction is not independent of genotype. Mechanistic models for chemical aspects of colorectal cancer and chemotherapy for breast cancer demonstrate some of the ways by which such interactions can be studied and the potential for future studies.
Molecular chaperones, stress proteins and redox homeostasis
Authors: Papp Eszter , Nardai Gábor , Söti Csaba , Csermely Péter 
Published: December 2008

AbstractProtection against oxidative stress is highly interrelated with the function of the most ancient cellular defense system, the network of molecular chaperones, heat shock, or stress‐proteins. These ubiquitous, conserved proteins help other proteins and macromolecules to fold or re‐fold and reach their final, native conformation. Redox regulation of protein folding becomes especially important during the preparation of extracellular proteins to the outside oxidative milieu, which should take place in a gradual and step‐by‐step controlled manner in the endoplasmic reticulum or in the periplasm. Several chaperones, such as members of the Hsp33 family in yeast and the plethora of small heat shock proteins as well as one of the major chaperones, Hsp70 are able to act against cytoplasmic oxidative damage. Abrupt changes of cellular redox status lead to chaperone induction. The function of several chaperones is tightly regulated by the surrounding redox conditions. Moreover, our recent data suggest that chaperones may act as a central switchboard for the transmission of redox changes in the life of the cell.
Redox signaling and the MAP kinase pathways
Authors: Torres Martine , Forman Henry Jay 
Published: December 2008

AbstractThe mitogen‐activated protein (MAP) kinases are a large family of proline‐directed, serine/threonine kinases that require tyrosine and threonine phosphorylation of a TxY motif in the activation loop for activation through a phosphorylation cascade involving a MAPKKK, MAPKK and MAPK, often referred to as the MAP kinase module. Three separate such modules have been identified, based on the TxY motif of the MAP kinase and the dual‐specificity kinases that strictly phosphorylate their specific TxY sequence. They are the extracellular signal regulated kinases (ERKs), c‐jun N‐terminal kinases (JNKs) and p38 MAPKs. The ERKs are mainly associated with proliferation and differentiation while the JNKs and p38MAP kinases regulate responses to cellular stresses.Redox homeostasis is critical for proper cellular function. While reactive oxygen species (ROS) and oxidative stress have been implicated in injury, a rapidly growing literature suggests that a transient increase in ROS levels is an important mediator of proliferation and results in activation of various signaling molecules and pathways, among which the MAP kinases. This review will summarize the role of ROS in MAP kinase activation in various systems, including in macrophages, cells of myeloid origin that play an essential role in inflammation and express a multi‐component NADPH oxidase that catalyzes the receptor‐regulated production of ROS.
Overview on coenzyme Q10 as adjunctive therapy in chronic heart failure. Rationale, design and end‐points of “Q‐symbio” ‐ A multinational trial
Authors: Mortensen Svend Aage 
Published: December 2008

AbstractEnergy starvation of the myocardium is probably a dominant feature of heart failure and attention has been directed towards agents which may stabilize myocardial metabolism and maintain adequate energy stores. A reduced myocardial tissue content of the essential redox‐component and natural antioxidant Coenzyme Q10 (CoQ10) has been detected in patients with heart failure and the observed level of CoQ10 deficiency was correlated to the severity of heart failure.CoQ10 fulfills various criteria of an obvious adjunct in patients with symptomatic heart failure: it is devoid of significant side effects and it improves symptoms and quality of life. Till this date, several double‐blind placebo‐controlled trials with CoQ10 supplementation in more than 1000 patients have been positive and statistically significant with respect to various clinical parameters, e.g. improvement in NYHA Class, exercise capacity and reduced hospitalisation frequency. Also treatment with CoQ10 led to a significant improvement of relevant hemodynamic parameters. In only 3 out of 13 double‐blind studies comprising 10% of the total number of patients treated the results were neutral. Thus, based on the available controlled data CoQ10 is a promising, effective and safe approach in chronic heart failure.This is why a double‐blind multicenter trial with focus on morbidity and mortality has been planned to start in 2003: Q‐SYMBIO. Patients in NYHA classes III to IV (N=550) receiving standard therapy are being randomized to treatment with CoQ10 100 mg t.i.d. or placebo in parallel groups. End‐points in a short‐term evaluation phase of 3 months include symptoms, functional capacity and biomarker status (BNP). The aim of a subsequent 2‐year follow‐up study is to test the hypothesis that CoQ10may reduce cardiovascular morbidity (unplanned cardiovascular hospitalisation due to worsening heart failure) and mortality as a composite endpoint. This trial should help to establish the future role of CoQ10 as part of a maintenance therapy in patients with chronic heart failure.
Relaxation of arterial smooth muscle: A new function of a water‐soluble degradation product of coenzyme Q (ubiquinone)
Authors: Bindu R. , Venkataraman B. V. , Rao Aparna V. S. , Ramasarma T. 
Published: December 2008

AbstractTreatment of coenzyme Q with ozone yielded a degradation product having unmodified ring that retained its spectral characteristics and a truncated side‐chain that made it water‐soluble. This derivative, but not the intact lipid‐quinone, showed relaxation of phenylephrine‐contracted rat arterial rings. This effect offers an explanation for the known hypotensive action of exogenous coenzyme Q regardless of its side‐chain length.
Derivatised α‐tocopherol as α CoQ10 carrier in a novel water‐soluble formulation
Authors: Sikorska Marianna , Borowy‐Borowski Henryk , Zurakowski Bogdan , Roy Walker P. 
Published: December 2008

AbstractWe have derivatised α‐tocopherol (vitamin E) to a water‐soluble polyoxyethanyl‐α ‐ tocopheryl sebacate (PTS) and discovered that it formed a non‐covalent complex with CoQ10 at a molar ratio of 2:1 (PTS‐CoQ10). This complex was water‐soluble and remained stable for extended periods of time. After oral delivery of the formulation into rats PTS was hydrolysed to vitamin E and elevated levels of both vitamin E and CoQ10 in blood plasma were detected within 1 h. Thus, this aqueous formulation contains a combination of two potent antioxidants. The formulation's efficacy was tested against ischemic brain damage caused by a transient (8∼min) bilateral occlusion of the common carotid arteries in rats. The animals received PTS‐CoQ10 by two intraperitoneal injections given immediately after ischemia and 3 h later and the brain damage was assessed up to 12 days post‐ischemia. A significant neuroprotection was observed in the CA1 hippocampal region, for example at 12 days approximately 50% of CA1 neurons were still alive in the treated animals versus less than 5% in the non‐treated group. Our data is consistent with previously published observations indicating the therapeutic potential of antioxidants for treatments of ischemia/reperfusion injuries and the formulation described here is particularly appropriate for the application in acute conditions, such as stroke or cardiac arrest.
Serum coenzyme Q10 concentrations in healthy men supplemented with 30 mg or 100 mg coenzyme Q10 for two months in a randomised controlled study
Authors: Zita Čestmír , Overvad Kim , Mortensen Svend Aage , Sindberg Christian Dan , Moesgaard Sven , Hunter Douglas A. 
Published: December 2008

AbstractSerum coenzyme Q10 (Q10) concentrations were evaluated in healthy male volunteers supplemented with 30 mg or 100 mg Q10 or placebo as a single daily dose for two months in a randomised, double‐blind, placebo‐controlled study. Median baseline serum Q10concentration in 99 men was 1.26 mg/l (10%, 90% fractiles: 0.82, 1.83). Baseline serum Q10 concentration did not depend on age, while borderline significant positive associations were found for body weight and smoking 1–10 cigarettes/d. Supplementation with 30 mg or 100 mg Q10 resulted in median increases in serum Q10 concentration of 0.55 mg/l and 1.36 mg/l, respectively, compared with a median decrease of 0.23 mg/l with placebo. The changes in the Q10 groups were significantly different from that in the placebo group, and the increase in the 100 mg Q10 group was significantly greater than that in the 30∼mg Q10 group. The change in serum Q10concentration in the Q10 groups did not depend on baseline serum 10 concentration, age, or body weight.
Cytoprotective and anticancer properties of coenzyme Q versus capsaicin
Authors: Galati Giuseppe , O'Brien Peter J. 
Published: December 2008

AbstractCoenzyme Q (CoQ) is an essential component of the mitochondrial electron transport chain and serves as an electron donor and acceptor in mitochondrial energy‐linked respiration. CoQ1was shown to prevent ROS formation and cell death in complex 1 inhibited cells. Low concentrations of capsaicin like CoQ1inhibited ROS formation but CoQ1was more effective at restoring the mitochondrial membrane potential collapse caused by complex 1 inhibitors such as rotenone. At low concentrations, capsaicin acts as a CoQ mimic by protecting against rotenone induced ROS formation and mitochondrial membrane potential collapse. Lipid peroxidation in isolated rat hepatocytes induced by cumene hydroperoxide and chloroacetaldehyde was also prevented. At higher concentrations, capsaicin and CoQ1became cytotoxic. Hep G2 cells were more susceptible than hepatocytes. The cytotoxic mechanism for both capsaicin and CoQ1was shown to involve a collapse of the mitochondrial membrane potential, however, only capsaicin caused ROS formation. The capsaicin side chain was required for capsaicin induced cytotoxicity. The anticancer properties of CoQ1and capsaicin should prove useful for inducing tumor cell apoptosis.
Pleiotropic phenotypes of fission yeast defective in ubiquinone‐10 production. A study from the abc1Sp (coq8Sp) mutant
Authors: Saiki Ryoichi , Ogiyama Yuki , Kainou Tomohiro , Nishi Tomoko , Matsuda Hideyuki , Kawamukai Makoto 
Published: December 2008

AbstractWe previously constructed two Schizosaccahromyces pombe ubiquinone‐10 (or Coenzyme Q10) less mutants, which are either defective for decaprenyl diphosphate synthase or p‐hydroxybenzoate polyprenyl diphosphate transferase. To further confirm the roles of ubiquinone in S. pombe, we examined the phenotype of the abc1Sp (coq8Sp) mutant, which is highly speculated to be defective in ubiquinone biosynthesis. We show here that the abc1Sp defective strain did not produce UQ‐10 and could not grow on minimal medium. The abc1Sp‐deficient strain required supplementation with antioxidants such as cysteine or glutathione to grow on minimal medium. In support of the antioxidant function of ubiquinone, the abc1Sp‐deficient strain is sensitive to H2O2 and Cu2+. In addition, expression of the stress inducible ctt1 gene was much induced in the ubiquinone less mutant than wild type. Interestingly, we also found that the abc1‐deficient strain as well as other ubiquinone less mutants produced a significant amount of H2S, which suggests that oxidation of sulfide by ubiquinone may be an important pathway for sulfur metabolism in S. pombe. Thus, analysis of the phenotypes of S. pombe ubiquinone less mutants clearly demonstrate that ubiquinone has multiple functions in the cell apart from being an integral component of the electron transfer system.