[Morphology and analysis of an acute lethal potassium dichromate--potassium ferricyanide-(3)-intoxication].
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Adult↗
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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↗
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↗
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↗
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↗
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↗
Failure of dialysis therapy in potassium dichromate poisoning.
A fatal case of oral ingestion of potassium dichromate is presented. Following an initial presentation of abdominal pain and vomiting, the patient had a rapid progression to coma with the development of methemoglobinemia, coagulopathy, gastrointestinal hemorrhage, and respiratory distress syndrome. A blood concentration of chromium on admission was 5,800 mcg/dL, 80% of which was found to be in the intracellular fraction. Supportive treatment was also initiated as a four-hour period of hemodialysis followed by a one-hour period of charcoal hemoperfusion. Neither of these treatment modalities was found to significantly remove chromium from whole blood and neither seemed to affect the progression or outcome of this intoxication. We conclude that the ingestion of potassium dichromate is highly toxic and may rapidly lead to death. Hemodialysis and charcoal hemoperfusion appear to have little role in the management of chromium intoxication.
Adolescent↗
Renal function in the rat after treatment with mercuric chloride plus potassium dichromate.
The treatment of rats with single subcutaneous (sc) doses of mercuric chloride (4 mg/kg) plus potassium dichromate (10 mg/kg) resulted in greater effects on water consumption, urine volume, body weight, and urinary electrolyte excretion than produced by mercuric chloride alone. The dose of potassium dichromate alone had no effects on renal function. Urine volume at 6 hr was increased twofold over mercuric chloride alone. Similarly, potassium excretion by these animals at 6 hr was significantly decreased compared to controls. These animals were oliguric by 24 hr after the injection. Urine osmolality of rats receiving the combination of the metals remained lower than controls throughout the 4-day experimental period. Measurement of renal arterial blood flow by electromagnetic flow probe after subcutaneous injection of saline, mercuric chloride (4 mg/kg), potassium dichromate (10 mg/kg), or the combination, produced no change over a 2.5-hr period, at 24 hr, and at 48 hr, and the glomerular filtration rate (GFR) of these rats was not affected over the same period of time.
Animals↗
Inhibition of DNA synthesis in BHK fibroblasts treated in vitro with potassium dichromate.
Treatment of hamster fibroblasts with potassium dichromate in vitro stimulates tritiated thymidine uptake into the intracellular nucleotide pool. This effect is due to the oxidizing action of hexavalent chromium on the plasma membrane. Dichromate, induces also an inhibition of DNA replication, which is due to the interaction of reduced trivalent chromium with specific biological ligands on the DNA molecule.
Cell Line↗
Effects of potassium dichromate and sample storage time on fat and protein by Milko-Scan and on protein and casein by a modified Pro-Milk Mk II method.
A rapid procedure is described for measuring casein in milk by a combination of isoelectric precipitation and amido black dye-binding. Individual milk samples from 38 cows were subsampled, preserved with potassium dichromate at a concentration of 8 mg/ml of milk, and analyzed for fat and protein by the Milko-Scan 300 and for protein and casein by the dye-binding procedure on day 1, 4, 7, and 10 after milk collection. Fat tests were not affected by sample storage time, but protein tests showed variation depending on the interval between milk sample collection and analysis. In a separate study effects of potassium dichromate used as a preservative at 0, 2, 4, 6, 8, and 12 mg/ml of milk on chemical determinations were investigated. No changes were significant in fat and protein analyzed by the infrared method for concentrations of preservative. There were no significant differences in protein determination by the two methods for nonpreserved samples. For preserved samples, the dye-binding method for protein gave determinations higher than those by the infrared method. The difference increased linearly with increasing concentration of potassium dichromate at .07% in protein for every 2 mg of potassium dichromate per milliliter of milk.
Animals↗
Conditions that influence the genetic activity of potassium dichromate and chromium chloride in Saccharomyces cerevisiae.
Potassium dichromate and chromium chloride were analyzed for their ability to induce mitotic gene conversion and point reverse mutation in D7 diploid strain of S. cerevisiae. We used cells from the stationary phase of growth with and without metabolic activation (S9 hepatic fraction) and cells from the logarithmic phase, that contain a high level of cytochrome P-450 and have a greater permeability. In the present work we confirmed the genetic activity of K2Cr2O7 in cells from the stationary phase, with and without S9 fraction and in cells from the logarithmic growth phase. A slight increase in genetic activity was observed in experiments with CrCl3 using phosphate buffer, but no genetic effects were noted in Tris-HCl buffer. Our studies suggest that phosphate ion may be the carrier responsible of the entrance of trivalent chromium in the cells. The higher cellular permeability may account for the different results obtained with both compounds in cells from the stationary and logarithmic phases of growth.
Biotransformation↗
Genotoxic effects of potassium dichromate, sodium arsenite, cobalt chloride and lead nitrate in diploid yeast.
4 metal salts, potassium dichromate, sodium arsenite, cobalt chloride and lead nitrate were tested for their genotoxic effects in Saccharomyces cerevisiae. Potassium dichromate was the most potent agent for induction of gene conversion and reverse mutation. Sodium arsenite was virtually ineffective as a convertogen but gave a positive result for reversion. Cobalt chloride was the least toxic, exhibited a convertogenic activity but was only marginally active for reverse mutation. Lead nitrate was the most toxic salt but was genetically inactive.
Arsenic↗
[Severe potassium dichromate poisoning after accidental nasal introduction].
BACKGROUND: Nasal foreign body (NFB) is a common situation in pediatrics. Poisoning is a rare complication of NFB insertion. We report a case of acute potassium dichromate poisoning secondary to NFB insertion. CASE REPORT: Six days after insertion of a NFB, progressive occurrence of diarrhea, vomiting, nasal obstruction, acute renal failure, pancreatitis, hepatitis and drowsiness justified hospitalization of a 3-year-old girl in the pediatric intensive care unit. Acute potassium dichromate poisoning was confirmed by high plasma chromium level and by the spectrophotometric analysis of the crystal. Recovery was satisfactory with supportive treatment. An official survey allowed to discover that the crystal was freely sold and that its toxicity was unknown by dealers, while no information was given to the customers. CONCLUSION: Transmucosal absorption of toxics is an unusual severe potential hazard that should be evoked to allow a rapid management. After the discovery and withdrawal of a NFB, occurrence of systemic symptoms, even trivial, must make one suspect a poisoning. In this circumstance, analysis of the foreign body should be done, associated with toxicologic dosages. This case report illustrates that potassium dichromate poisoning is a severe medical condition and that its clinical presentation assume a large widespread of symptoms due to multiple organ involvement.
Absorption↗