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At least 685 records · Page 38Linked to original sources
PubMed1995

Inhibition of citrate lyase may aid aerobic endurance.

Owing to a substantial increase in glucose uptake by working muscle, glucose homeostasis during sustained aerobic exercise requires a severalfold increase in hepatic glucose output. As exercise continues and liver glycogen declines, an increasing proportion of this elevated glucose output must be provided by gluconeogenesis. Increased gluconeogenic efficiency in trained individuals is a key adaptation promoting increased endurance, since failure of hepatic glucose output to keep pace with muscle uptake rapidly leads to hypoglycaemia and exhaustion. Pre-administration of (-)-hydroxycitrate, a potent inhibitor of citrate lyase found in fruits of the genus Garcinia, may aid endurance during post-absorptive aerobic exercise by promoting gluconeogenesis. Carnitine and bioactive chromium may potentiate this benefit. The utility of this technique may be greatest in exercise regimens designed to promote weight loss.

Aerobiosis↗
PubMed1985

External beam pelvic radiotherapy plus intraperitoneal radioactive chronic phosphate in early stage ovarian cancer: a toxic combination. A National Cancer Institute of Canada Clinical Trials Group Report.

As part of a randomized trial evaluating several treatment programs in the management of poor prognosis, early stage ovarian cancer, 53 patients were randomized to receive a combination of pelvic external beam radiation, 4000 rad plus 10-20 millicuries of radioactive chromic phosphate given intraperitoneally. Only 35 patients (66%) actually received the chromic phosphate. The other 18 did not enter this phase of treatment for a variety of reasons documented in this report. Ten (29%) of the 35 patients receiving the full course of treatment had significant long term side effects with the median time to onset of symptom being 9 months after the chronic phosphate was given. There were no treatment-related deaths. The complications could not be related to the dose of the isotope, the technique of administration, nor any other definable predisposing factors. This combination is not recommended for further study.

Brachytherapy↗
PubMed1988

Peritoneal fluid cytology in endometrial cancer: its significance and the role of chromic phosphate (32P) therapy.

Between 1978 and 1986, 243 patients (all stages) had peritoneal fluid cytology performed while undergoing total abdominal hysterectomy for endometrial carcinoma; 39 (16%) were found to be positive. At 3 years (median follow-up of 30 months) the disease-free survival (DFS) for the 165 negative cytology clinical Stage I patients was 91% compared to only 56% for the 25 positive cytology patients (p less than .001). Of the 25 Stage I positive cytology patients, 14 with greater than one-third myometrial invasion had a DFS of 30% at 3 years as compared to 87% for negative cytology patients with comparable depth of invasion (p less than .001). There was no difference in DFS between the negative and positive cytology Stage I patients who had one-third or less myometrial invasion. Stage I patients with histologic Grade 2 and 3 had a lower 3 year DFS when cytology positive, 49% and 22%, versus 92% and 79% when cytology negative (p less than .001 and p = .03 respectively). In clinical Stage II patients the 3-year DFS was 21% for those with a positive cytology and 59% with a negative cytology. Fourteen of the 25 clinical Stage I positive cytology patients received 15 mCi of intraperitoneal 32P. At 3 years they had a 68% DFS as compared to 27% for those not receiving 32P (p = 0.01). All 11 patients with superficial myometrial invasion (9 received 32P) remained disease-free. The 4 Stage I patients with deep invasion who received 32P therapy had an improvement in abdominal/pelvic control and DFS when compared to 9 similar patients who did not receive 32P (p = .02). For histologic Grade 2 and 3 patients, there was a 64% 3-year DFS in the 32P treated group and 16% for those not receiving 32P (p = 0.02). Although 32P therapy improved DFS in Stage I positive cytology patients its use along with pelvic radiation therapy can lead to complications. Of 9 Stage I patients receiving 32P as well as pelvic irradiation, 4 experienced serious bowel complications requiring surgery. None of the 5 patients receiving 32P only had a complication.

Ascitic Fluid↗
PubMed1991

Intraperitoneal radioactive phosphate in early ovarian carcinoma: an analysis of complications.

Intraperitoneal radioactive chromic phosphate was administered to 69 patients with Stage I and II ovarian carcinoma who had undergone comprehensive surgical staging. Intestinal obstruction requiring surgical intervention occurred in four patients and was the most severe complication. Abdominal pain was the most common post-therapy complaint. Attention to time and technique of drug administration could minimize complications.

Adolescent↗
PubMed1982

Subchronic oral toxicity and analytical studies on nickel rutile yellow and chrome rutile yellow with rats.

The inorganic pigments nickel rutile yellow and chrome rutile yellow were fed to groups of 15 male and 15 female rats each for 3 months at dietary levels of 0, 10, 100, 1000 and 10000 ppm, respectively. On an additional 5 animals each, levels of nickel and antimony or chromium and antimony in liver and kidneys, respectively, were measured after 1 and 2 months. Appearance, behaviour, food consumption, growth, mortality, haematological and clinical chemical data, organ weights, and gross and micromorphology of organs were not affected in any dose group. In livers and kidneys antimony median levels below 30 ppb were detectable only in the group of rats fed the highest level of 10000 ppm of the two pigments.

Animals↗
PubMed1995

Chromium-induced excretion of urinary lipid metabolites, DNA damage, nitric oxide production, and generation of reactive oxygen species in Sprague-Dawley rats.

Chromium and its salts induce cytotoxicity and mutagenesis, and vitamin E has been reported to attenuate chromate-induced cytotoxicity. These observations suggest that chromium produces reactive oxygen species which may mediate many of the untoward effects of chromium. We have therefore examined and compared the effects of Cr(III) (chromium chloride hexahydrate) and Cr(VI) (sodium dichromate) following single oral doses (0.50 LD50) on the production of reactive oxygen species by peritoneal macrophages, and hepatic mitochondria and microsomes in rats. The effects of Cr(III) and Cr(VI) on hepatic mitochondrial and microsomal lipid peroxidation and enhanced excretion of urinary lipid metabolites as well as the incidence of hepatic nuclear DNA damage and nitric oxide (NO) production were also examined. Increases in lipid peroxidation of 1.8- and 2.2-fold occurred in hepatic mitochondria and microsomes, respectively, 48 hr after the oral administration of 25 mg Cr(VI)/kg, while increases of 1.2- and 1.4-fold, respectively, were observed after 895 mg Cr(III)/kg. The urinary excretion of malondialdehyde (MDA), formaldehyde (FA), acetaldehyde (ACT) and acetone (ACON) were determined at 0-96 hr after Cr administration. Between 48 and 72 hr post-treatment, maximal excretion of the four urinary lipid metabolites was observed with increases of 1.5- to 5.4-fold in Cr(VI) treated rats. Peritoneal macrophages from Cr(VI) treated animals 48 hr after treatment resulted in 1.4- and 3.6-fold increases in chemiluminescence and iodonitrotetrazolium reduction, indicating enhanced production of superoxide anion, while macrophages from Cr(III) treated animals showed negligible increases. Increases in DNA single strand breaks of 1.7-fold and 1.5-fold were observed following administration of Cr(VI) and Cr(III), respectively, at 48 hr post-treatment. Enhanced production of NO by peritoneal exudate cells (primarily macrophages) was monitored following Cr(VI) administration at both 24 and 48 hr post-treatment with enhanced production of NO being observed at both timepoints. The results indicate that both Cr(VI) and Cr(III) induce an oxidative stress at equitoxic doses, while Cr(VI) induces greater oxidative stress in rats as compared with Cr(III) treated animals.

Acetaldehyde↗
PubMed1996

Hodgkin's disease in association with hexavalent chromium exposure.

During an epidemiological study assessing cancer risk in a small isolated population exposed to excessive amounts of hexavalent chromium, we noted two patients with Hodgkin's disease after exposure for many years and after a long latency period. The study population demonstrated an observed risk between 65 and 92 times that of reported risks for non-exposed US populations. Although malignant lymphoma, as well as many other malignancies, has clearly been associated with hexavalent chromium exposure, no reports have yet specifically mentioned Hodgkin's disease. We herein report Hodgkin's disease specifically in two individuals so exposed. Although this may be a chance occurrence, clinicians should be aware of the potential association between hexavalent chromium exposure and Hodgkin's lymphoma.

Adult↗
PubMed1994

139La nuclear magnetic resonance characterisation of La2O3 and La1-xSrxMO3 where M = Cr, Mn or Co.

139La Nuclear magnetic resonance (NMR) spectra have been used to obtain nuclear quadrupole coupling parameters for La2O3 and a series of perovskites La1-xSrxMO3 (where M = Cr, Mn or Co). Depending on the doping level of SrO2 these materials are either paramagnetic or ferromagnetic at room temperature. Magnetic transferred hyperfine effects are strongly in evidence in the Mn compounds. A 59Co NMR spectrum was observed in LaCoO3. A precision measurement of the nuclear quadrupole coupling constant in La2O3 was made by nuclear quadrupole resonance (NQR) spectroscopy.

Calcium Compounds↗
PubMed2006

Oxidation of trichloroethene over metal oxide catalysts: kinetic studies and correlation with adsorption properties.

The performance of bulk chromium oxide is compared with that of a Mn commercial catalyst for the deep oxidation of trichloroethene (1000-2500ppmv, 55h(-1) space velocity) in air, in dry and wet (20000ppm of H(2)O) conditions, in terms of activity, selectivity and stability. Chromium oxide was found to be more active (on a catalyst weight basis), however its activity decreases continuously with time on stream. The presence of water increases its stability, the Mn catalyst showing the opposite behaviour. The effect of water on the Cr catalyst can be explained according to the Deacon equilibrium, as the presence of water tends to decrease the Cl(2) concentration, assumed to be responsible of the catalyst deactivation. Regarding to the selectivity, the Mn catalyst yields C(2)Cl(4), CCl(4) and CHCl(3) as organochlorinated by-products, whereas chromium oxide produces only trace amounts of CCl(4). Simple power-law kinetics expressions (first-order for Mn and zero-order for Cr) provide fairly good fits for the evolution of the conversion with the temperature. Furthermore, the kinetic behaviour of chromium oxide can be represented with a Langmuir-Hinshelwood model taking into account the chlorine inhibitory effect.

Adsorption↗
PubMed2006

Both trivalent and hexavalent chromium strongly alter in vitro germination and ultrastructure of kiwifruit pollen.

Due to its widespread industrial use, chromium is considered a dangerous environmental pollutant. It is known to inhibit plant growth and development. The present study provides the first evidence of the toxicity of this metal on the male haploid generation of a higher plant. Both Cr(III) and Cr(VI) species, supplied as CrCl(3) and CrO(3), respectively, exerted a strong dose-dependent inhibitory effect on kiwifruit pollen tube emergence and growth. Cr(III) resulted more effective than Cr(VI) in the 16-75microM interval; moreover, complete inhibition of germination was attained at much lower doses than Cr(VI). Also tube morphology was affected. While the plasma membrane was still undamaged in the large majority of the treated pollen grains, dramatic ultrastructural alterations were induced by chromium including chromatin condensation, swelling of mitochondria, cytoplasmic vacuolization, and perturbed arrangement of endoplasmic reticulum cisternae. Thus, it seems that the impact of the two chromium species on kiwifruit pollen may result in severe compromission of both essential structures and functions of the male gametophyte.

Actinidia↗
PubMed2006

Salt effects on aggregation of O-carboxymethylchitosan in aqueous solution.

The effects of salt with different valences (NaCl, CaCl2 and CrCl3) on the aggregation of O-carboxylmethylchitosan (OCMCS) in dilute aqueous solution were investigated using viscometry, dynamic laser light scattering (DLS) and atomic force microscopy (AFM). With increasing OCMCS concentration beyond a critical aggregation concentration (cac) of approximately 0.045 g/l, the aggregation of OCMCS appears in solution. The driving forces of the OCMCS aggregation are intermolecular hydrogen bond, hydrophobic interaction and electrostatic repulsion. The OCMCS aggregation behavior strongly depends on the valence of salt. When NaCl is added, the aggregate size increases with NaCl concentration. When CaCl2 or CrCl3 is added to a given OCMCS concentration, there exists a critical concentration each of Ca2+ and Cr3+. Before the critical concentration, the aggregates decrease in size with increasing salt concentration due to the intra-aggregate complexation; while after the critical concentration, the size of the aggregates increases with salt concentration due to the inter-aggregate complexation. Moreover, the effect of Cr3+ on the OCMCS aggregation is greater than that of Ca2+. The formation of the intra-aggregate complexation is found to be a kinetic process and the aggregate size decreases with time; the formation of the inter-aggregate complexation is also kinetic where the aggregate size increases with time. The aggregates dominated by the intra-aggregate complexation are small, compact and spherical, while the aggregates dominated by the inter-aggregate complexation show the big, compact and spherical morphology.

Calcium Chloride↗
PubMed2005

Recognition of the oxidized lesions spiroiminodihydantoin and guanidinohydantoin in DNA by the mammalian base excision repair glycosylases NEIL1 and NEIL2.

8-Oxoguanine (8-oxoG) is an unstable mutagenic DNA lesion that is prone to further oxidation. High valent metals such as Cr(V) and Ir(IV) readily oxidize 8-oxoG to form guanidinohydantoin (Gh), its isomer iminoallantoin (Ia), and spiroiminodihydantoin (Sp). When present in DNA, these lesions show enhanced base misincorporation over the parent 8-oxoG lesion leading to G --> T and G --> C transversion mutations and polymerase arrest. These findings suggested that further oxidized lesions of 8-oxoG are more mutagenic and toxic than 8-oxoG itself. Repair of oxidatively damaged bases, including Sp and Gh/Ia, are initiated by the base excision repair (BER) system that involves the DNA glycosylases Fpg, Nei, and Nth in E. coli. Mammalian homologs of two of these BER enzymes, OGG1 and NTH1, have little or no affinity for Gh/Ia and Sp. Herein we report that two recently identified mammalian glycosylases, NEIL1 and NEIL2, showed a high affinity for recognition and cleavage of DNA containing Gh/Ia and Sp lesions. NEIL1 and NEIL2 recognized both of these lesions in single-stranded DNA and catalyzed the removal of the lesions through a beta- and delta-elimination mechanism. NEIL1 and NEIL2 also recognized and excised the Gh/Ia lesion opposite all four natural bases in double-stranded DNA. NEIL1 was able to excise the Sp lesion opposite the four natural bases in double-stranded DNA, however, NEIL2 showed little cleavage activity against the Sp lesion in duplex DNA although DNA trapping studies show recognition and binding of NEIL2 to this lesion. This work suggests that NEIL1 and NEIL2 are essential in the recognition of further oxidized lesions arising from 8-oxoG and implies that these BER glycosylases may play an important role in the repair of DNA damage induced by carcinogenic metals.

Animals↗
PubMed2004

Protective effects of 17beta-estradiol and trivalent chromium on interleukin-6 secretion, oxidative stress, and adhesion of monocytes: relevance to heart disease in postmenopausal women.

Postmenopausal diabetic women are at greater risk for heart disease compared with men of similar age and with other risk factors. We examined the hypothesis that 17beta-estradiol and trivalent chromium inhibit secretion of the pro-inflammatory cytokine interleukin (IL)-6 and oxidative stress in monocytes exposed to high glucose (HG). U937 human monocytes were cultured with HG (30 mM) with and without 17beta-estradiol (0-1000 nM) and chromium chloride (Cr(3+), 0-10 muM) at 37 degrees C for 24 h. Results show that 17beta-estradiol inhibits IL-6 and adhesion to endothelial cells (p <. 05) by HG-treated monocytes. Treatment with 17beta-estradiol+Cr(3+) required a significantly lower dose of estradiol-17beta compared with 17beta-estradiol alone for IL-6 inhibition. 17beta-Estradiol+Cr(3+) also inhibited lipid peroxidation and the adhesivity to human endothelial cells in HG-treated monocytes. Thus, 17beta-estradiol+Cr(3+) inhibits oxidative stress, IL-6 secretion, and monocytic adhesion to endothelial cells, risk factors in the development of heart disease. The female body requires E but studies on some patients indicate side effects with increased amounts of 17beta-estradiol-supplementation. The potential benefit of a lower estrogen dose in combination with chromium is novel and needs to be explored in postmenopausal diabetic women.

Antioxidants↗
PubMed2005

Cytotoxicity studies of chromium(III) complexes on human dermal fibroblasts.

The cytotoxicity of certain Cr(III) complexes, such as [Cr(salen)(H(2)O)(2)](+), [Cr(edta)(H(2)O)](-), [Cr(en)(3)](3+), [Cr(ox)(3)](3-), [Cr(pic)(3)], and CrCl(3), which differ in ionic character and ligand environment in human dermal skin fibroblasts, has been studied. After 72 h of exposure to 100 microM doses of chromium(III) complexes, the order in which the complexes had an inhibitory effect on cell viability was [Cr(en)(3)](3+) > [Cr(salen)(H(2)O)(2)](+) > [Cr(ox)(3)](3-) > [Cr(edta)(H(2)O)](-) > [Cr(pic)(3)] > CrCl(3). Based on viability studies it was confirmed that [Cr(en)(3)](3+), a triply charged cation, inhibits cell proliferation, and therefore, it was chosen to carry out further investigations. [Cr(en)(3)](3+), at a dose of 50 microM, was found to bring about surface morphological changes, evidenced by cellular blebbing and spike formation accompanied by nuclear damage. TEM analysis revealed substantial intracellular damage to fibroblasts in terms of the formation of apoptotic bodies and chromatin condensation, thus reflecting cell death. FACS analysis further revealed DNA damage by formation of a sub-G(1) peak with 84.2% DNA as aneuploid DNA and arrest of the G(2) / M phase of the cell cycle. Cellular DNA damage was confirmed by agarose gel electrophoresis with the characteristic appearance of a DNA streak in DNA isolated from [Cr(en)(3)](3+)-treated fibroblasts. The proposed mechanism suggests the plausible role of Cr(V), formed as a result of oxidation of Cr(III) by cellular oxidative enzymes, in the cytotoxic response. Consequently, any Cr(III) complex that is absorbed by cells and can be oxidized to Cr(V) must be considered a potential carcinogen. This has potential implications for the increased use of Cr(III) complexes as dietary supplements and highlights the need to consider the cytotoxicity and genotoxicity of a variety of Cr(III) complexes and to understand the potential hazards of Cr(III) complexes encountered in research laboratories.

Apoptosis↗
PubMed2005

The role of oxidative stress in the modulation of aryl hydrocarbon receptor-regulated genes by As3+, Cd2+, and Cr6+.

Heavy metals alter the capacity of AhR ligands to induce the bioactivating phase I and the detoxifying phase II xenobiotic-metabolizing enzymes but the mechanism(s) remain unknown. In the present study, we evaluated the role of As(3+)-, Cd(2+)-, and Cr(6+)-induced oxidative stress on the expression of Cyp1a1, Nqo1, and Gst ya in Hepa 1c1c7 cells. Both Cd2+ and Cr6+, but not As3+, increased the production of ROS. However, all metals increased cellular GSH content and heme oxygenase-1 mRNA levels. Although all three metals inhibited the induction of Cyp1a1 activity by TCDD, Cyp1a1 mRNA levels were potentiated. When cellular GSH was depleted with buthionine-(S,R)-sulfoximine (BSO), Cyp1a1 mRNA expression was further potentiated whereas Cyp1a1 activity was further inhibited. In parallel, pretreatment with the antioxidant N-acetylcysteine (NAC) did not alter Cyp1a1 mRNA expression but completely abrogated the inhibition of Cyp1a1 activity induction by all three metals. On the other hand, all three metals, alone or in the presence of TCDD, enhanced Nqo1 and Gst ya mRNA levels and Nqo1 activity. These effects were potentiated in the presence of BSO and abrogated with NAC. Our data clearly show that As(3+)-, Cd(2+)-, and Cr(6+)-induced oxidative stress modulates Cyp1a1 at transcriptional and posttranscriptional levels but induces Nqo1 and Gst ya at the transcriptional level.

Acetylcysteine↗
PubMed2006

Evaluation of immunotoxic and immunodisruptive effects of inorganic arsenite on human monocytes/macrophages.

A trivalent inorganic arsenic, arsenite, has been causing chronic inflammation in humans through the consumption of contaminated well water. The total peripheral blood arsenic concentrations of chronic arsenic-exposed patients, who had inflammatory-like immune responses, are less than 1 microM, thus, nM concentrations may be very important regarding the chronic inflammatory effects by arsenite. However, there are few reports about the biological effects of low concentrations of arsenite in mammalian cells, especially in normal immune effector cells. In this study, we examined whether arsenite has any biological and/or toxicological effects on the differentiation of human peripheral blood monocytes into macrophages using the colony-stimulating factor (CSF) in vitro compared with that of other metallic compounds, and found that arsenite sensitively inhibited the CSF-induced in vitro maturation of monocytes into macrophages at nM levels, and it also induced small, nonadhesive and CD14-positive abnormal macrophage generation from monocytes with granulocyte-macrophage CSF (GM-CSF) at 50-500 nM without cell death. The addition of other metallic compounds, including chromium, selenium, mercury, cadmium, nickel, copper, zinc, cobalt, manganese and other human pentavalent arsenic metabolites, such as inorganic arsenate, monomethylarsonic acid and dimethylarsinic acid, could not induce the same abnormal cell generation from monocytes with CSFs at any concentration and any additional time schedules; they showed only simple cytolethality in monocytes and macrophages at any concentration and any additional time schedules; they showed only simple cytolethality in monocytes and macrophages at n-mM levels accompanied by cell death. This work may have implications in the arsenic-induced chronic inflammation in humans.

Arsenites↗