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PubMed2000

Permeability, cytotoxicity, and genotoxicity of Cr(III) complexes and some Cr(V) analogues in V79 Chinese hamster lung cells.

The permeabilities and genotoxicities of the Cr(III) complexes [Cr(en)(3)](3+), mer-[Cr(glygly)(2)](-), cis-[Cr(phen)(2)(OH(2))(2)](3+), and trans-[Cr(salen)(OH(2))(2)](+) and the Cr(V) analogues of cis-[Cr(phen)(2)(OH(2))(2)](3+) and trans-[Cr(salen)(OH(2))(2)](+) [en being 1,2-ethanediamine, glygly being glycylglycine, phen being 1,10-phenanthroline, and salen being N,N'-ethylenebis(salicylideneiminato)] have been studied in V79 Chinese hamster lung cells. Following exposure of approximately 10(6) cells to 0.4 mM Cr(III) for 4 h, the Cr uptake by single cells was less than 10(-)(14) g/cell (as determined by GFAAS analysis and as confirmed by PIXE analysis where the Cr concentration was below the limit of detection). Importantly, the Cr(V) analogue of cis-[Cr(phen)(2)(OH(2))(2)] was significantly more permeable than the Cr(III) complex. The cytotoxicity of the Cr(III) complexes increased in the following order: mer-[Cr(glygly)(2)](-) < [Cr(en)(3)](3+) approximately cis-[Cr(phen)(2)(OH(2))(2)](3+) < trans-[Cr(salen)(OH(2))(2)](+). No genotoxic effects were observed following exposure to mer-[Cr(glygly)(2)](-) or [Cr(en)(3)](3+) at concentrations up to 6 mM. The Cr(III) imine complexes trans-[Cr(salen)(OH(2))(2)](+) and cis-[Cr(phen)(2)(OH(2))(2)](3+), which could be oxidized to Cr(V) complexes, induced MN in vitro at rates of 13.6 and 3.3 MN/1000 BN cells/micromol of Cr, respectively. The comparative permeabilities and genotoxicities of trans-[Cr(salen)(OH(2))(2)](+) and [CrO(salen)](+) were similar due to the instability of the Cr(V) complex at physiological pH values (7.4). There was a substantial increase in the permeability of [Cr(O)(2)(phen)(2)](+), compared to that of the Cr(III) analogue, which was accompanied by a highly genotoxic response. Consequently, any Cr(III) complex that is absorbed by cells and can be oxidized to Cr(V) must be considered as 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 genotoxicities of a variety of Cr(III) complexes when determining the carcinogenic potential of Cr(III) particularly when "high" deliberately administered doses are concerned.

Animals↗
PubMedDate not supplied

Reaction of chromium(VI) with ascorbate produces chromium(V), chromium(IV), and carbon-based radicals.

Reaction of potassium dichromate with sodium ascorbate was studied by EPR spectroscopy at room temperature, in 0.10 M N-[2-hydroxyethyl]piperazine-N'-[2-ethanesulfonic acid] (HEPES), phosphate, cacodylate, and tris(hydroxymethyl)aminomethane hydrochloride (Tris.HCl) buffers at pH 7.0, in the presence of 0.10 M spin trap [5,5-dimethyl-1-pyrroline 1-oxide or 2-methyl-N-(4-pyridinylmethylene)-2-propanamine N,N'-dioxide]. Chromium(V), ascorbate radical, CO2-, and other carbon-based spin trap-radical adducts were observed. Chromium(V), CO2-, and the carbon-based radicals were observed at low ratios of ascorbate to chromium, and ascorbate radical was observed at high ratios of ascorbate to chromium. The presence of Cr(IV) was detected indirectly by reaction with Mn(II) and a subsequent decrease in the Mn(II) EPR signal. More Cr(IV) was found for the higher reaction ratios of ascorbate to Cr(VI). The only buffer effect observed was a relative decrease of the Cr(V) signal in Tris.HCl vs HEPES, phosphate, and cacodylate buffers, no change in the radical adducts was observed. There was no evidence for reactive oxygen species an intermediates in this reaction. Addition of the singlet oxygen trap 2,2,6,6-tetramethyl-4-piperidone hydrochloride showed no 2,2,6,6-tetramethyl-1-piperidinyloxy radical formation. The Cr(V) species did not react with dioxygen, and dioxygen did not affect the formation of carbon-based radicals. A mechanism consistent with these observations is discussed.

Ascorbic Acid↗
PubMed2002

Genotoxicity of trivalent chromium in bacterial cells. Possible effects on DNA topology.

Trivalent chromium is a metal required for proper sugar and fat metabolism. However, it has been suggested that it causes DNA damage in in vitro test systems, although in vivo toxicity has not yet been proved. In the present study, the effect of Cr3+ on bacterial cells was tested with the Pro-Tox (C) assay, and its cellular uptake was measured with flame atomic absorption spectroscopy. The potential genotoxicity of Cr3+ was further examined by the study of its influence on a bacterial type II topoisomerase. Cr3+ was shown to cause DNA damage and inhibit topoisomerase DNA relaxation activity, probably by preventing the formation of the covalent link between enzyme and double helix. In addition, Cr3+ decreases the viability and/or proliferation rate of eukaryotic cells such as murine B16 melanoma cells and human MCF-10A neoT ras-transformed human epithelial cells. The possible implication for Cr3+ intake by humans is discussed.

Animals↗
PubMed2003

Characterization of nonmutagenic Cr(III)-DNA interactions.

Exposure of cells or animals to carcinogenic chromium(VI) (Cr(VI)) produces Cr(III)-DNA adducts. The relevance of these lesions to Cr(VI)-induced tumors is unclear. Various Cr(III) complexes have been used to model the products resulting from Cr(VI) metabolism in order to gain mechanistic insights. The purpose of this study was to characterize interactions of Cr(III) complexes with DNA in order to evaluate their use as models for these purposes. The reactivity of DNA with chromic chloride hexahydrate (CrCl(3)) and sodium bis(l-cysteinato)chromium(III) dihydrate (Cr(cys)(2)(-)) was compared to that with cis-diamminedichloroplatinum(II) (cis-platin). Both Cr(III) and Pt(II) cause unwinding of supercoiled DNA that can be visualized as a mobility shift by gel electrophoresis. Chromic chloride was much less distorting than cis-platin, unwinding DNA by only 1-2 degrees, and Cr(cys)(2)(-) interacted with DNA only weakly. Consistent with in vitro studies, CrCl(3) produced Cr-DNA adducts in CHO AA8 cells at levels equivalent to those obtained with Cr(VI), whereas Cr(cys)(2)(-) did not produce significant adducts. Lesions produced by CrCl(3) were not mutagenic in the hypoxanthine-Gua-phosphoribosyl-transferase assay. These data are consistent with CrCl(3) producing a nondistorting lesion, perhaps by association with the phosphate backbone. There are two possible interpretations of these results: Either the Cr(III) products formed by Cr(VI) metabolism are not modeled by CrCl(3) and Cr(cys)(2)(-) complexes, or Cr(III) is not an active species for Cr(VI)-induced DNA damage. This study provides the first structural evidence for Cr(III)-DNA adducts. A molecular understanding of Cr(III)-DNA interactions will be necessary before we can determine their relevance in Cr(VI)-induced cancers.

Animals↗
PubMed1997

Direct and hydrogen peroxide-induced chromium(V) oxidation of deoxyribose in single-stranded and double-stranded calf thymus DNA.

Oxidative DNA damage by a model Cr(V) complex, [CrO(ehba)2]-, with and without added H2O2, was investigated for the formation of base and sugar products derived from C1', C4', and C5' hydrogen atom abstraction mechanisms. EPR studies with 5,5-dimethylpyrroline N-oxide (DMPO) have shown that Cr(V)-ehba alone can oxidize the spin trap via a direct chromium pathway, whereas reactions of Cr(V)-ehba in the presence of H2O2 generated the hydroxyl radical. Direct (or metal-centered) Cr(V)-ehba oxidation of single-stranded (ss) and double-stranded (ds) calf thymus DNA demonstrated the formation of thiobarbituric acid-reactive species (TBARS) and glycolic acid in an O2-dependent manner, consistent with abstraction of the C4' H atom. A minor C1' H atom abstraction mechanism was also observed for direct Cr(V) oxidation of DNA, but no C5' H atom abstraction product was observed. Direct Cr(V) oxidation of ss- and ds-DNA also caused the release of all four nucleic acid bases with a preference for the pyrimidines cytosine and thymine in ds-DNA, but no base release preference was observed in ss-DNA. This base release was O2-independent and could not be accounted for by the H atom abstraction mechanisms in this study. Reaction of Cr(V)-ehba with H2O2 and DNA yielded products consistent with all three DNA oxidation pathways measured, namely, C1', C4', and C5' H atom abstractions. Cr(V)-ehba and H2O2 also mediated a nonpreferential release of DNA bases with the exception of the oxidatively sensitive purine, guanine. Direct and H2O2-induced Cr(V) DNA oxidation had opposing substrate preferences, with direct Cr(V) oxidation favoring ss-DNA while H2O2-induced Cr(V) oxidative damage favored ds-DNA. These results may help explain the carcinogenic mechanism of chromium(VI) and serve to highlight the differences and similarities in DNA oxidation between high-valent chromium and oxygen-based radicals.

Animals↗
PubMed1998

Permeability, cytotoxicity, and genotoxicity of chromium (V) and chromium (VI) complexes in V79 Chinese hamster lung cells.

The genotoxicity of Cr(V) complexes in mammalian cells (V79 Chinese hamster lung cells) has been studied for the first time using the in vitro micronucleus assay. Two complexes were investigated, [CrO(ehba)2]-, which undergoes ligand-exchange and disproportionation reactions in the cell growth medium, and [CrO(mampa)]-, which is chemically inert in the medium for the duration of the exposure period. Results of in vitro micronucleus assays show that both complexes are genotoxic and exhibit similar potencies to that of [Cr2O7]2-. The permeabilities of the Cr(V) complexes were also investigated for the first time using particle-induced X-ray emission (PIXE) analysis of individual cells. The Cr uptake increased in the order: [Cr(phen)2-(H2O)2]3+ < [CrO(ehba)2]- < [CrO(mampa)]- < [Cr2O7]2-. Clonal assays showed that Cr(VI) exhibits an expectedly higher cytotoxicity than the Cr(V) complexes. While the genotoxicities of the Cr(V) and Cr(VI) complexes increase according to their permeabilities, the genotoxicities of the Cr(V) complexes are equal to, if not greater than, that of Cr(VI) in terms of the amount of Cr entering the cell. This supports other evidence that Cr(V), produced as a metabolic intermediate from the intracellular reduction of Cr(VI), may be important in Cr-induced cancers.

Animals↗
PubMed2000

Second primary malignancies following the treatment of early stage ovarian cancer: update of a study by the National Cancer Institute of Canada--Clinical Trials Group (NCIC-CTG).

BACKGROUND: Ovarian cancer is the leading cause of death from gynecological malignancies and the fourth most frequent fatal malignancy in women. Despite improved surgical techniques as many as 20% of women with early stage disease will eventually relapse and die from their disease. The post-operative management of these women remains controversial. Here we present the long term follow-up data of our previously published study, as well as the incidence of second primary malignancies in these women. PATIENTS AND METHODS: Two hundred fifty-seven eligible patients with stage I, IIA 'high risk' ovarian carcinoma and IIB, IIIO (disease confined to pelvis) were randomized to either whole abdominal radiotherapy 2.250 rads in ten fractions (107 patients), melphalan 8 mg/m2/d x 4 weeks x 18 courses (106 patients) or intraperitoneal chromic phosphate 10-20 mCi (44 patients). All patients were initially treated with pelvic radiotherapy. RESULTS: Overall survival estimates at 10 years were: 45% in the whole abdominal radiotherapy arm; 49% in the melphalan arm and 50% in the intraperitoneal chromic phosphate arm (P = 0.30). Relapse-free survival estimates at 10 years were: 50% in the whole abdominal radiotherapy arm, 62% in the melphalan arm and 51% in the chromic phosphate arm (P = 0.147). Long term follow-up has not demonstrated a significant difference between treatment arms. Second primary malignancies developed in 29 women (11%) after 2,229 person years of follow-up. This compares to 18.7 second primary malignancies which would have been expected in this group of age-matched controls and was statistically significant (P = 0.018). There was no significant difference in the total number of second primary malignancies between treatment arms. Melphalan appeared to be associated with an increased risk of developing leukemia/myelodysplastic syndrome compared to the whole abdominal radiotherapy arm (P = 0.06). CONCLUSIONS: Long-term follow-up has not demonstrated a significant difference in overall or disease free survival between treatment arms. An excess of second primary malignancies (35%) was observed suggesting that lifelong surveillance is required in this population. Further research with newer treatment programs are needed to improve the cure rates in this population.

Antineoplastic Agents, Alkylating↗
PubMed2001

Combining Drosophila melanogaster somatic-mutation-recombination and electron-spin-resonance-spectroscopy data to interpret epidemiologic observations on chromium carcinogenicity.

Lung cancers are significantly increased among workers exposed to chromate (Cr6+, Cr3+), chromium pigments (Cr6+) and chromium plating (Cr6+). Chromium lung burdens and cancer risk increase proportionately with duration of employment at long latencies. However, this epidemiologic information alone is insufficient in determining whether Cr6+ or Cr3+ are equally important in causing cancer. We have attempted to combine epidemiologic data with data from the Drosophila melanogaster somatic-mutation-recombination-test and from the in vitro electron-spin-resonance spectroscopy study to demonstrate that following somatic recombination plays a more important role than somatic mutation in chromium carcinogenesis. Cr4+ is more important than Cr5+ or Cr6+ in inducing somatic recombination while Cr6+ produces more and bigger clones than Cr4+ in somatic mutation. Cr3+ produces negative results in this fruit-fly wing-spot-assay. When the larvae and flies exposed to Cr6+ and Cr4+ are examined by ESR, only Cr5+ and Cr3+ are found. Thermodynamic parameters deltaE, deltaH, and deltaS are also estimated from these latter experiments to explain the relative importance of Cr6+, Cr4+, Cr3+ in chromium carcinogenesis among exposed industrial workers.

Animals↗
PubMed2004

Caspase-3: its potential involvement in Cr(III)-induced apoptosis of lymphocytes.

In this study, we have examined the role of caspase-3 in apoptosis of lymphocytes induced by the chromium(III) complexes viz. tris-(1,10-phenanthroline)chromium(III) chloride (Cr(III)-phen) and trans-diaqua[1,3-bis(salicylideneamino)propanechromium(III)] perchlorate (Cr(III)-salprn). Evidence for caspase-3 activation and poly(ADP-ribose) polymerase (PARP) cleavage in lymphocytes exposed to Cr(III) complexes is revealed through Western blotting analysis. Blocking the activity of caspase-3 with z-DEVD-fmk, prevents apoptosis as evidenced through [3H]-thymidine incorporation, DNA fragmentation assay and measurement of sub-G1 cells by flow cytometry. Pretreatment of lymphocytes with free radical scavengers completely attenuates the activity of caspase-3 suggesting that reactive oxygen species (ROS) are upstream activators of caspase-3. Preincubation of lymphocytes with PP2, a selective Src-family tyrosine kinase inhibitor, abolishes the activation of caspase-3 indicating that Src-family tyrosine kinases viz. p56lck, p59fyn and p53/56lyn are mediators of caspase-3 activation during Cr(III) exposure. Collectively, our findings support a plausible mechanism in which Cr(III) mediates ROS generation that precedes the up-regulation of p56lck, p59fyn and p53/56lyn which eventually activates caspase-3 to promote apoptotic cell death of lymphocytes. To our knowledge, this is the first report suggesting the importance of Src-family tyrosine kinases for the activation of caspase-3 in metal-induced apoptotic cell death.

Apoptosis↗
PubMed2001

Autoxidation and toxicant-induced oxidation of lipid and DNA in monkey liver: reduction of molecular damage by melatonin.

Melatonin, the main secretory product of the pineal gland, is a free radical scavenger and antioxidant which protects against oxidative damage due to a variety of toxicants. However, there is little information regarding melatonin's antioxidative capacity in tissues of primates. In this study we examined the protective effects of melatonin in monkey liver homogenates against lipid damage that occurred as a result of autoxidation or that induced by exogenous addition of H202 and ferrous iron (Fe2+). Additionally, we tested melatonin's protective effect against oxidative damage to DNA induced by chromium(III) (CrIII) plus H202. The levels of malondialdehyde and 4-hydroxyalkenals were assayed as an index of lipid peroxidation, and the concentrations of 8-hydroxydeoxyguanosine (8-OHdG) as an endpoint of oxidative DNA damage. The increases in malondialdehyde+4-hydroxyalkenals concentrations as a consequence of autoxidation or after the addition of H202 plus Fe2+ to the homogenates were time-dependent. The accumulation of these damaged products due to either auto-oxidative processes or induced by H202 and Fe2+ were significantly reduced by melatonin in a concentration-dependent-manner. The levels of 8-OHdG were elevated in purified monkey liver DNA incubated with a combination of CrCl3 plus H2O2. This rise in oxidatively damaged DNA was prevented by 10 microM concentration of melatonin. Also, melatonin reduced the damage to DNA that was caused by auto-oxidative processes. These findings in monkey liver tissue document the ability of melatonin to protect against oxidative damage to both lipid and DNA in primate tissue, as observed previously in rodent tissue. The findings provide support for the use of melatonin as suitable agent to reduce damage inflicted by free radical species in primates.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2006

Carrier-controlled ferromagnetism in transparent oxide semiconductors.

The search for an ideal magnetic semiconductor with tunable ferromagnetic behaviour over a wide range of doping or by electrical gating is being actively pursued as a major step towards realizing spin electronics. A magnetic semiconductor having a high Curie temperature, capable of independently controlled carrier density and magnetic doping, is crucial for developing spin-based multifunctional devices. Cr-doped In(2)O(3) is such a unique system, where the electrical and magnetic behaviour-from ferromagnetic metal-like to ferromagnetic semiconducting to paramagnetic insulator-can be controllably tuned by the defect concentration. An explicit dependence of magnetic interaction leading to ferromagnetism on the carrier density is shown. A carrier-density-dependent high Curie temperature of 850-930 K has been measured, in addition to the observation of clear magnetic domain structures in these films. Being optically transparent with the above optimal properties, Cr-doped In(2)O(3) emerges as a viable candidate for the development of spin electronics.

Alloys↗
PubMed1999

Treatment of malignant pericardial effusion with 32P-colloid.

Malignant pericardial effusion is usually treated only when signs of cardiac tamponade develop. Several methods of treatment have been reported with an overall response rate of approximately 75%. Since our initial study using intrapericardial 32P-colloid instillation as a treatment modality for pericardial effusion demonstrated a significant higher response rate, this study was conducted to further evaluate the efficacy of intrapericardial 32P-colloid in terms of response rates and duration of remissions. Intrapericardial instillation of 185-370 MBq (5-10 mCi) 32P-colloid in 36 patients with malignant pericardial effusion resulted in a complete remission rate of 94.5% (34 patients) whereas two patients did not respond to treatment due to a foudroyant formation of pericardial fluid. The median duration time was 8 months. No side-effects were observed. These results suggest that intrapericardial instillation of 32P-colloid is a simple, reliable and safe treatment strategy for patients with malignant pericardial effusions. Therefore, since further evidence is provided that 32P-colloid is significantly more effective than external radiation or non-radioactive sclerosing agents, this treatment modality should be considered for the management of malignant pericardial effusion.

Breast Neoplasms↗
PubMed1986

Lactulose, 51Cr-labelled ethylenediaminetetra-acetate, L-rhamnose and polyethyleneglycol 400 [corrected] as probe markers for assessment in vivo of human intestinal permeability.

The urinary excretion of lactulose, 51Cr-labelled ethylenediaminetetra-acetate (51Cr-EDTA), L-rhamnose and polyethyleneglycol 400 (PEG-400) has been measured after intravenous and oral administration in healthy volunteers. Intestinal permeation of the probes was compared after their ingestion in iso-osmolar, hyperosmolar and cetrimide-containing test solutions. Urinary recovery of lactulose and 51Cr-EDTA after intravenous administration reached 75% by 5 h, and exceeded 90% at 24 h, and these values were 62 and 72%, respectively, for L-rhamnose. Recovery of PEG-400, however, varied with the relative molecular mass (Mr) of each polymer from 25.9 to 68.5% in 24 h. Intestinal permeation of ingested lactulose and 51Cr-EDTA was low, but that of L-rhamnose was 45-fold, and that of PEG-400 100-fold, greater. Permeation of lactulose and 51Cr-EDTA was markedly increased by cetrimide and hyperosmolar stress, whereas that of L-rhamnose showed little change. PEG-400 permeation was not affected by cetrimide, but was slightly increased by hyperosmolar stress. The 5 h permeation of lactulose, but not of L-rhamnose or PEG-400, correlated with that of 51Cr-EDTA (r = 0.98, P less than 0.001). These findings are compatible with three distinct pathways of unmediated mucosal permeation, L-rhamnose (radius less than 0.4 nm) passing mainly through small aqueous 'pores' of high incidence, lactulose and 51Cr-EDTA (radius greater than 0.5 nm) through larger aqueous 'channels' of low incidence susceptible to cetrimide and hyperosmolar stress, and PEG-400, which has appreciable lipid solubility, by partition through cell membrane lipid as well as the aqueous 'pores'.

Cell Membrane Permeability↗
PubMed2001

32P chromic phosphate radiosynovectomy for chronic haemophilic synovitis.

The principal medical consequence of haemophilia is the development of arthropathy, initiated by a haemarthrosis giving rise to chronic synovitis. Traditional methods of synovectomy include open excision and arthroscopy each of which require substantial amounts of clotting factor concentrate for several weeks, and in the case of open synovectomy, is often associated with loss of range of motion and arthrofibrosis. Radiosynovectomy, the intra-articular injection of low penetration radiocolloids, has been utilized outside the United States for over 20 years. Since 1988, our centre has performed 170 radiosynovectomies utilizing 32P chromic phosphate (32P). This study reports results of 130 32P radiosyovectomies with an average follow-up of 36.5 months (6-140 months). For primary procedures, excellent and good results (haemarthrosis reduction from 75 to 100%) were obtained in 79.2% of cases at 6 months to 8 years. For repeat procedures a combination of excellent and good results were obtained in 62.4% of cases at 6 months to 3 years. Regression analysis showed no correlation between results and age or degree of arthropathy. Radiation was well contained within the joint. There were no observed or identified complications. The procedure is highly cost effective in comparison to open surgical or arthroscopic synovectomy.

Adolescent↗
PubMed1999

In vitro cytotoxicity of fibre-polymethyl methacrylate composite used in dentures.

The aim of this study was to determine the in vitro cytotoxicity of fibre-polymethyl methacrylate (PMMA) composite used in denture bases. Both heat-cured and autopolymerized PMMA were tested as the matrix of the fibre composite or as a plain denture polymer. The fibres tested included unsized E-glass and silica fibres, silica fibres which were sized with a silane coupling agent only, as well as commercially epoxy-silane or methacrylate-chrome complex sized E-glass fibres. The indirect contact cytotoxicity test by agar diffusion was carried out according to the international standard ISO 10993-5 after storing the test specimens in water for 24 h. PVC plastic was used as a positive control and polyethylene plastic was used as a negative control. Within the limitations of the agar diffusion test, it can be concluded that neither the unreinforced PMMA nor the fibre composite made from PMMA and fibres was cytotoxic.

Animals↗