[Morphology and analysis of an acute lethal potassium dichromate--potassium ferricyanide-(3)-intoxication].
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Adult↗
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Results for “Potassium Dichromate”
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Delayed-type hypersensitivity reaction in the lungs of guinea pigs due to potassium dichromate.
Potassium dichromate was inhaled by guinea pigs previously immunized by potassium dichromate until strong positive patch tests were obtained. No obvious respiratory changes were noted during and after inhalation. Histologically, however, mononuclear cells infiltrated the interstitial spaces in large areas of the lung, producing considerable thickening of the alveolar spaces in 24 to 48 hr after inhalation. Polymorphonuclear cells were predominant initially. These changes were similar to the delayed-type hypersensitivity reaction in the lung elicited by the inhalation of purified protein derivative (PPD) in the guinea pigs immunized by an injection of dry-killed tubercle bacilli. A less marked reaction was observed in guinea pigs passively sensitized with peritoneal exudate cells and lymph node cells. Consequently, the pulmonary changes were thought to be elicited by delayed-type hypersensitivity reaction due to a simple chemical. The clinical implications of delayed-type hypersensitivity reaction in the lung due to simple chemicals are discussed.
Administration, Intranasal↗
Fixation of proteins by osmium tetroxide, potassium dichromate and potassium permanganate. Model experiments with bovine serum albumin and bovine gamma-globulin.
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Animals↗
The protective role of thiola and soybean seeds against the genotoxicity induced by potassium dichromate in mice.
The genotoxic potential of potassium dichromate (K(2)Cr(2)O(7)) was evaluated in vivo in mice using different mutagenic end points. Chromosomal aberrations in bone-marrow and spermatocytes as well as sperm abnormalities in the tested mice were determined. The doses used were 3, 6, 12 mg K(2)Cr(2)O(7)kg(-1) body weight which correspond to 1/16, 1/8, 1/4 the experimental LD(50), respectively. The protective roles of i.p. injection with thiola (a synthetic sulfhydryl compound) at 20 mg kg(-1) body weight and feeding treatment with soybean seeds (30% of the diet) were also studied. For chromosomal aberration analysis, subacute treatment for a period of 3 weeks were performed. All the tested doses of K(2)Cr(2)O(7) induced a statistically significant increase in the percentage of chromosomal aberrations in both somatic and germ cells with dose and time relationships. The percentage of the induced chromosomal aberrations was significantly minimized in all groups of mice i.p. treated with thiola or fed soybean seeds during the period of treatment. Potassium dichromate also induced a significant increase (P<0.01) in the percentage of abnormal sperms at the doses 6 and 12 mg kg(-1) body weight. Such percentage reached 7.52+/-0.45, 5.50+/-0.53 and 4.28+/-0.45 in mice treated with the highest tested dose of K(2)Cr(2)O(7), K(2)Cr(2)O(7) and thiola; K(2)Cr(2)O(7) and soybean, respectively compared with 2.14+/-0.33 for the control. In conclusion, the results demonstrate the genotoxic effect of potassium dichromate in mice. The results also confirm the protective role of thiola and soybean seeds against the genotoxicity of potassium dichromate.
Animals↗
[Study on teratogenic effect of potassium dichromate on Vicia faba root tip cells].
We studied the aberrant effects of different concentrations of potassium dichromate on Vicia faba root tip cells. The micronucleus and chromosome aberration assay was conducted to determine the micronucleus rate and chromosome aberration rate of Vicia faba root tip cells induced by potassium dichromate. The result indicated that potassium dichromate could increase the micronucleus rate of Vicia faba root tip cells. Within certain range of concentration the rate of micronucleus was found to be increased with the increase of potassium dichromate concentration,but beyond this range the rate of micronucleus decreased with further increase of potassium dichromate concentration. The potassium dichromate at different concentrations could increase the cell mitosis index. Besides,it also caused various types of chromosome aberration,and the rates of chromosome aberration were always higher than that of the control group. The conclusion of this study was that potassium dichromate has obvious teratogenic effect on Vicia faba root tip cells.
Chromosome Aberrations↗
Contact sensitization of mice to nickel sulphate and potassium dichromate.
The ability of nickel sulphate and potassium dichromate to induce contact sensitization in mice has been investigated. Topical exposure of mice to 0.5% potassium dichromate in dimethylsulphoxide (DMSO) under occlusion resulted in specific contact sensitization in each of 7 experiments. Although sensitization to nickel sulphate under the same conditions was weak and somewhat variable, evidence for significant levels of contact allergy was obtained in 4 of 7 experiments. In addition, repeated topical application of both nickel sulphate and potassium dichromate in DMSO was found to result in the induction of lymphocyte proliferative responses in lymph nodes draining the site of exposure. These data indicate that epicutaneous exposure to both metal salts may cause specific contact sensitization in mice.
Animals↗
Interaction of potassium dichromate with the nephrotoxins, mercuric chloride and citrinin.
Potassium dichromate enhanced the effects of mercuric chloride or citrinin on renal slice transport of the organic ions p-aminohippurate (PAH) and tetraethylammonium (TEA) under certain experimental conditions. At the doses employed and times studied no effects, or only minimal effects, were observed on renal slice transport when the toxins were tested individually. Potassium dichromate (10 mg/kg) administered subcutaneously (s.c.) in combination with mercuric chloride (4 mg/kg, s.c.) or citrinin 35 or 55 mg/kg administered intraperitoneally (i.p.), resulted in a marked depression of organic ion transport. Similarly, the addition of potassium dichromate to fresh renal cortex slices in combination with mercuric chloride, enhanced the mercuric chloride-induced reduction of transport. No other interactions were observed under in vitro conditions.
Animals↗
Changes in leucine transport activity in Chironomus riparius larvae after short-term exposure to potassium dichromate and fenitrothion.
The effect of sublethal concentrations of potassium dichromate and fenitrothion on sodium-leucine cotransport in brush border membrane vesicles from Chironomus riparius larvae has been investigated. Exposure to potassium dichromate and fenitrothion caused a dose- and time-dependent inhibition of leucine uptake. Transport inhibition is easily detectable at doses 100-fold lower than LD50. Kinetic experiments showed that inhibition was mainly caused by a decrease of the Vmax (680 +/- 53 vs. 382 +/- 23 and 555 +/- 27 nmol/15s/mg protein in control and exposed larvae to K2Cr2O7 and fenitrothion, respectively). Inhibition is possibly related to a variation of sodium ions permeability as evidenced by increased membrane lipid peroxidation. Appropriate control experiments ruled out that the observed differences could be due to changes in general features of membrane preparations. Transport inhibition observed in larvae exposed to potassium dichromate was accompanied by changes in ascorbate peroxidase and dehydroascorbate reductase activities, whereas those exposed to fenitrothion displayed an increase in transaminase activity. The possible value of leucine uptake as biochemical biomarker is briefly discussed. Arch. Insect Biochem. Physiol. 55:90-101, 2004.
Amino Acid Transport Systems↗
[Study of DNA damage induced by potassium dichromate and glutathione with atomic force microscope].
OBJECTIVE: To observe calf thymus DNA damage induced by potassium dichromate in combination with glutathione (GSH). METHODS: Atomic force microscope and ultraviolet spectrum (UV) were used to observe the alterations of the DNA ultrastructure and absorption spectrum. RESULTS: Atomic force microscopy revealed no breaks of the DNA strand in response to treatment with potassium dichromate alone, but when coupled with GSH at proper concentrations, potassium dichromate induced alterations in the DNA structure and DNA fragmentation. UV examination also confirmed these findings by showing increased absorption intensity of the maximum UV peak following combined treatment of the DNA with potassium dichromate and GSH. CONCLUSION: These morphological and spectrographic evidences verified the important role of GSH in mediating the generation of various tumor-inducing intermediate products of potassium dichromate.
Animals↗
Successful treatment of a patient suffering from severe acute potassium dichromate poisoning with liver transplantation.
BACKGROUND: Oral ingestion of potassium dichromate produces a complex spectrum of complications. It has an extremely poor prognosis and usually leads to rapid death. METHODS: We report the case of a 16-year-old male patient who was admitted to hospital after oral ingestion of potassium dichromate with suicidal intention. RESULTS: The patient's condition deteriorated, and he became comatose within 5 days in spite of immediate attempts at detoxification. Because of irreversible liver failure, which occurred within 2 days after admission, and because of cerebral edema, the decision to perform a liver transplantation was made. On day 6 after admission, a compatible donor liver was transplanted. The course of liver transplantation and the patient's subsequent recovery were uneventful. CONCLUSION: The rationale for the delayed transplantation was to avoid damage of the new organ because of high serum chromium levels. Despite severe organ damage, the chromium content of the liver was increased. To the authors' knowledge, this is the first case report of acute toxic liver failure, caused by potassium dichromate poisoning, treated successfully by means of liver transplantation.
Acute Disease↗
Antigenotoxic properties of selenium compounds on potassium dichromate and hydrogen peroxide.
Selenium is an environmental metal that occurs ubiquitously and is produced throughout the world for various industrial activities. Selenium has been reported to have anticarcinogenic and preventive effects in clinical and epidemiological studies. Selenium supplements can inhibit chemically-induced tumours. From the viewpoint of genotoxicity, selenium has not been adequately studied and an IARC review concluded that there were not sufficient data to consider it a carcinogen for man. In contrast, hexavalent chromium is classified as a known respiratory carcinogen producing DNA damage through free oxygen radicals. In the present study, a collaborative study has been carried out to evaluate the genotoxicity of selenium compounds and their possible interactions with potassium dichromate and hydrogen peroxide. Thus, in laboratory 1 (U.K.), the genotoxic effects of three selenium compounds were examined. Sodium selenate, sodium selenite, and selenous acid were investigated in the Ames test using strain TA102 and in the Comet assay using human lymphocytes, and also investigated for their interaction with potassium dichromate. In the Ames test, it was shown that potassium dichromate produced a highly mutagenic response, whilst the three selenium compounds did not. In combination, sodium selenate reduced the genotoxicity of potassium dichromate, but sodium selenite and selenous acid had no effect. In the Comet assay, potassium dichromate induced DNA damage, but so did the selenium compounds. In combination with potassium dichromate, however, only sodium selenate reduced its effect, whereas sodium selenite and selenous acid exacerbated DNA damage. In laboratory 2 (Spain), in the TK6 lymphoblastoid cell line, the Comet assay showed that sodium selenite was non-genotoxic, while potassium dichromate and hydrogen peroxide induced DNA damage. It was also shown that sodium selenite did not decrease the genotoxicity of potassium dichromate or hydrogen peroxide when administered as a pre-treatment or at the same time, or when potassium dichromate and sodium selenite treatments were for different time periods. Thus, only sodium selenate has shown antigenotoxic properties against potassium dichromate in the Ames test and in human lymphocytes in the Comet assay.
Comet Assay↗
Poisoning with a traditional remedy containing potassium dichromate.
A fatal case of potassium dichromate ingestion is documented. A retrospective review of serum and organ levels of chromium demonstrates that charcoal haemoperfusion, peritoneal and haemodialysis are ineffective therapies for the toxin. Other treatments for this poisoning are reviewed, the poor prognosis of dichromate ingestion, and the paucity of effective therapy underlined. The application of dichromates in traditional medications is briefly discussed; this is a toxin which may be more prevalent than previously thought. It is proposed that the exposure limits of dichromate be more widely publicised.
Autopsy↗
Thioguanine resistance, ouabain resistance and sister chromatid exchanges in V79/AP4 Chinese hamster cells treated with potassium dichromate.
The biological activity of potassium dichromate (K2Cr2O7) was assayed in V79/AP4 Chinese hamster cells by measuring two mutational end points, thioguanine (TG) resistance and ouabain (OUA) resistance, and two non-mutational end points, cytotoxicity and sister chromatid exchanges (SCE). By exposing the cells for 1 h to the chemical, all biological end points examined were affected by the treatment in a dose-dependent manner. Moreover the combined use of the two selective systems indicated that chromium induces base-pair substitutions in mammalian cells in culture.
Animals↗
Genetic and DNA-methylation changes induced by potassium dichromate in Brassica napus L.
This study evaluated genetic and DNA methylation alteration induced by potassium dichromate in Brassica napus L. plants. Amplified fragment length polymorphism (AFLP) and selective amplification of polymorphic loci (SAMPL) tests revealed dose-related increases in sequence alterations in plantlets exposed to 10-200 mg/l potassium dichromate. Individual plantlets exposed to chromium under similar conditions showed different AFLP and SAMPL DNA profiles. These observations suggest random DNA mutation in response to potassium dichromate and argue against preferential sites for mutation. DNA methylation changes in response to chromium treatment were also evaluated. Two complementary approaches were applied: (i) immunolabelling, using a monoclonal antibody against 5-methylcytosine; and (ii) methylation-sensitive amplified polymorphism (MSAP). Immunolabelling showed cytosine-hypermethylation in the Brassica napus L. genome when plants were treated with potassium dichromate. MSAP analysis showed extensive methylation changes in CCGG-sequences, with the net result being genome-wide hypermethylation. These results showed a clear DNA alteration in plants as a response to chromium exposure and the effect was dose-dependent. DNA polymorphism detected by different markers supports the effectiveness of the use of these tools for the investigation of environmental toxicology and for evaluating the concentration of pollutants by DNA analysis in plants.
Analysis of Variance↗
[Detecting the DNA damage of N-ras gene induced by potassium dichromate].
OBJECTIVE: Applying RDPCR to detect the DNA damage of N-ras gene induced by Potassium dichromate METHODS: Preparing single-stranded probes of exon 1 of N-ras gene in human. The genomic DNA was treated with Potassium dichromate, then amplified by RDPCR and detected by Southern hybridization with the probe. RESULTS: The clear hybridized bands can be seen in the position which is induced by Potassium dichromate on the dose of 100 micromol/L, but can't be detected on the dose over 1000 mol/L. CONCLUSION: It indicates that Potassium dichromate can cause the DNA damage of N-ras gene, which should be the key point of its carcinogenesis mechanisms.
DNA Damage↗
Investigation of ability of the metal allergens cobalt chloride, nickel sulfate and potassium dichromate to give a mitogenic response in human thymocytes.
The metal allergens cobalt chloride, nickel sulfate and potassium dichromate were tested for the ability to give a mitogenic response in human thymocytes, both unseparated and Percoll-separated, including a fraction of low density, which has been shown to have characteristics of medullary cells (unsensitized, virgin T cells). With cobalt chloride and potassium dichromate, no stimulation occurred; instead, cobalt chloride at a concentration of 3.5 X 10(-5) M and potassium dichromate at 5.7 X 10(-7) M were inhibiting. After nickel sulfate addition, a small DNA synthesis stimulation was obtained in both unseparated cells and in fractionated cells of different densities. The results thus speak against that cobalt chloride and potassium dichromate are unspecific mitogens for human lymphoid cells, while an unspecific mitogenic effect is indicated for nickel sulfate.
Allergens↗
Chromate-allergic patients challenged orally with potassium dichromate.
30 patients who had positive patch tests to potassium dichromate participated in a placebo-controlled oral challenge with 2.5 mg chromium given as potassium dichromate. 17 reacted to chromate but not to the placebo, 2 reacted to both chromate and the placebo, and 4 reacted to the placebo but not chromate. 7 patients had no reaction. A specific reaction to chromate was most common among patients with dermatitis of the hands and/or feet.
Administration, Oral↗
The use of potassium dichromate and ethyl alcohol as blood preservatives for analysis of organochlorine contaminants.
The "gold standard" for preserving and shipping of human tissue samples for analysis of organochlorine contaminants is freezing. This method can be difficult, costly if using heavy dry ice for shipping, and often unfeasible, especially in less developed countries where electricity and dry ice are frequently rare or absent. Therefore, it is essential that more convenient and practical methods for preservation of blood samples are found. As an alternative to freezing, there have been studies employing potassium dichromate as a preservative for human or cow's milk or ethyl alcohol preservation of blood for dioxin analysis. In this study, four methods were compared to investigate the effectiveness of ethyl alcohol and potassium dichromate as blood preservatives for analysis of dioxins, dibenzofuran, and polychlorinated biphenyl (PCB) congeners. Samples of whole blood from a Dallas, Texas hospital were collected and pooled. Freezing, ethyl alcohol in two concentrations (20% and 40% per volume of sample), and potassium dichromate were used for blood preservation. The blood samples containing potassium dichromate or ethyl alcohol were stored and sent to ERGO laboratory for dioxin analysis and comparison with results from the frozen sample, which was kept frozen at all times until analyzed. This study suggests that potassium dichromate is a suitable alternative to freezing for preservation of whole blood for dioxin, dibenzofuran, and PCB measurements when either lipid or wet weight based results are reported. Potassium dichromate tablets were very easy and convenient to use--two 100 mg tablets (with a dichromate content of about 33 mg each) were added to each bottle containing 65 ml of blood. However, ethyl alcohol at 20% and 40% concentration under the conditions of this pilot study and the analytical method employed did not appear to provide satisfactory preservation when lipid based results are given or when the fat content has to be determined (wet or whole weight). Further research with a larger number of samples, inclusion also of other groups of persistent organic pollutants such as organochlorine pesticides or brominated flame retardants, a longer duration of storage time, and at temperatures greater than US or German room temperature is indicated in order to recommend the routine use of potassium dichromate as preservative for whole blood intended for dioxin, dibenzofuran, and PCB analysis.
Blood Preservation↗