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Biomedical subjects

F W Sunderman

Publications and source records attributed to F W Sunderman.

At least 235 records · Page 13Linked to original sources
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Perils of mercury.

The historical items pertaining to mercury are outlined, and its toxicity and former medicinal uses are discussed. The diversity of the toxic effects by the different forms of mercury as well as the routes of administration are illustrated in three case reports. The importance of diaphoresis in the treatment of mercury poisoning as well as the status of the use of chelating agents are reviewed. The need for the surveillance of mercury and the prevention of exposure to mercury from environmental and dietary sources are emphasized. The importance of excluding mercury toxicity in patients with psychiatric and neurological disorders is stressed.

Humans↗
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A review of the metabolism and toxicology of nickel.

Although nickel is an essential element for animal nutrition, the physiological role of nickel is not yet established. Pathological alterations of nickel metabolism are recognized in several human diseases. The diverse clinical manifestations of nickel toxicology include: (1) acute pneumonitis from inhalation of nickel carbonyl, (2) chronic rhinitis and sinusitis from inhalation of nickel aerosols, (3) cancers of nasal cavities and lungs in nickel workers, and (4) dermatitis and other hypersensitive reactions from cutaneous and parenteral exposures to nickel alloys. The toxicity, carcinogenicity and embryotoxicity of nickel compounds in experimental animals are reviewed in this article, and consideration is given to the therapeutic use of chelating drugs in nickel poisoning.

Abnormalities, Drug-Induced↗
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Hypernickelemia following coronary arteriography, caused by nickel in the radiographic contrast medium.

Meglumine diatrizoate ("Renografin-76", a radiographic contrast medium) contains sufficient nickel to cause hypernickelemia in patients after coronary arteriography. Nickel analyses by electrothermal atomic absorption spectrophotometry showed that nine lots of "Renografin-76" (760 g of meglumine diatrizoate per L) contained 144 +/- 44 micrograms Ni per L. Serum Ni concentrations became elevated in 11 patients after coronary arteriography (Ni dose = 19 +/- 4 micrograms per patient); peak Ni concentrations (increment = 1.8 +/- 0.4 micrograms Ni per L) occurred 0.25 or 0.5 h post-injection. Serum Ni concentrations diminished at 2 and 4 h post-injection and returned to base-line values at 24 h. The half-time (T1/2) for reduction of serum Ni concentrations averaged 1.5 h. Analysis of urine specimens from two patients showed that most of the Ni dose was excreted in urine within 24 hours. After iv administration of meglumine diatrizoate to rabbits (0.5 or 1.0 micrograms Ni per kg body wt), T1/2 values for elimination of Ni from the serum volume averaged 1.2 h, compared to T1/2 values of 5.7 and 7.4 h, respectively, when Ni was administered iv in NiCl2 or albumin solutions. Since "Renografin-76" contains edetate disodium (0.4 g per L), Ni is probably present as a Ni-EDTA complex, accounting for the rapid elimination of Ni following iv administration of the contrast medium to patients and rabbits. To reduce possible hazards of allergic or cardiovascular reactions to nickel, the authors recommend that Ni concentrations in radiographic contrast media should not exceed 10 micrograms per L.

Adult↗
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Histogenesis of subcutaneous malignant tumors resulting from nickel subsulfide implantation.

Tumors are described which have been produced by subcutaneous (s.c.) implantation of nickel subsulfide (Ni3S2) in 00 gelatin capsules in the left axillary region of Fischer 344 rats. This is in contradistinction to previous accounts where intramuscular (i.m.) or, in a few cases, subcapsular testicular implantation sites have been used. The advantages of the s.c. route are discussed, including the removal of the difficulties of distinguishing degenerating and regenerating striated muscle cells from tumor cells. The s.c. induced tumors were transplanted as far as the F6 generation, in some cases. Cells from tumor transplanted as far as the F3 generation were grown in tissue culture and then reimplanted s.c. Cytology of the tumors remained remarkably constant in all tumors, even after serial transplants and culture. A characteristic storiform pattern, with two major cell types -myofibroblasts and histiocyte-like cells, was seen. The question of pluripotential cell origin is discussed. The striking similarity of appearance to human malignant fibrous histiocytoma is noted; however, in view of the somewhat controversial origin of the human tumor, the simple designation, "nickel-induced malignant tumor of pluripotential origin", is preferred. The use of this model with its demonstrated ability to reproduce characteristic appearances seems to be valuable for the study of soft tissue sarcomas.

Animals↗
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Rapid analysis of nickel in urine by electrothermal atomic absorption spectrophotometry.

A method is described for analysis of nickel in urine, which involves dilution of urine with dilute nitric acid and direct quantitation of nickel by electrothermal atomic absorption spectrophotometry with Zeeman background correction. The detection limit for nickel is 0.5 micrograms per L of urine; the coefficient of variation of replicate determinations is 4 to 5 percent (within-run) and 6 percent (run-to-run). Recovery of nickel added to urine (20 micrograms per L) averages 99 +/- 5 percent (mean +/- SD). Analytical results agree closely with measurements by the International Union of Pure and Applied Chemistry (IUPAC) reference procedure (correlation coefficient = 0.99). Nickel concentrations in urine specimens from 34 non-exposed, healthy, adult persons living in Connecticut average 2.0 +/- 1.5 microgram per L (range = 0.5 to 6.0 micrograms per L). Urine nickel concentrations are directly correlated with urine creatinine concentrations and specific gravity measurements. Elevated concentrations of nickel are observed in urine specimens from nickel-exposed workers, including nickel electroplating workers (mean = 27 micrograms per L, range = 3.1 to 82 micrograms per L, N = 19) and nickel battery workers (mean = 32 micrograms per L, range = 2.8 to 103 micrograms per L, N = 7). This method is more rapid and convenient than previous techniques and is suitable for routine use in clinical and industrial laboratories.

Creatinine↗
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Ethene (ethylene) and ethane exhalation in Ni[II]-treated rats, using an improved rebreathing apparatus.

To assess the effects of NiCl2 on lipid peroxidation, exhalation rates of ethene (ethylene) and ethane were measured in Fischer-344 rats, using modifications of a recently published rebreathing apparatus and gas chromatographic assay. Technical improvements included more efficient removal of H2O vapor, NH3, and CO2, use of economical, readily available components, convenient standardization procedure, and no necessity for a charcoal concentrator accessory for the gas chromatograph. The detection limit was one pmol ethene or ethane per five mL air sample; the within-run precision (CV) of analysis was 2.1 percent at an ethane concentration of 16 pmol per five mL sample. A minimum of eight hours post-injection was necessary for exhalation rates of ethene or ethane to become significantly increased in NiCl2-treated rats. Ethene exhalation rate was increased 2.0- to 3.5-fold at 13 to 16 and 20 to 23 hours after NiCl2 injection (0.50 or 0.75 mmol per kg, body wt, sc). Ethane exhalation rate was increased 1.5- to 1.6-fold at the lower dosage, but was not significantly increased at the higher dosage of NiCl2. This study corroborates previous reports that lipid peroxidation is enhanced in target tissues (liver, kidney, lung) of NiCl2-treated rats.

Animals↗
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Historical review and assessment of clinical hemoglobinometry in the United States.

An historical review of clinical hemoglobinometry has been presented. Investigators who have made important contributions to our knowledge of hemoglobin have been cited. A questionnaire was distributed to 750 clinical laboratories in the United States to ascertain (a) the type of instrumentation used routinely to measure hemoglobin; (b) the methods that are now being used for clinical hemoglobinometry; (c) reference material that is used for daily quality control; and (d) the methods used for primary standardization. The results of the 263 responses to the questionnaire are reported. It is noteworthy that at the present time, 78 percent of the responding laboratories use the same instrumentation system. An assessment has been made of the precision of hemoglobin measurements undertaken in clinical laboratories in the United States over the past four decades. The data indicate that hemoglobin measurements during the past four years have become significantly more precise. There is probably no single factor responsible for this timely improvement; however, it may be inferred that the shift from manual to automated methodology in recent years is an important contributing factor.

Europe↗
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Increased lipid peroxidation in tissues of nickel chloride-treated rats.

Parenteral administration of nickel chloride (NiCl2) to rats enhanced lipid peroxidation in liver, kidney, and lung (but not in brain, heart, spleen, or testis), as measured by the thiobarbituric acid reaction for malondialdehyde (MDA) and related chromogens in fresh tissue homogenates. After sc injection of NiCl2 (0.75 mmol per kg body wt), MDA concentrations in liver and kidney became significantly increased by nine h and reached peak values at 48 h. For example, in nine rats killed 48 h after the NiCl2 injection, hepatic MDA concentrations averaged 2.5 +/- 1.0 mumol per g dry wt (P less than 0.001 versus 0.5 +/- 0.3 mumol per g in 30 controls). Dose-effect relationships for lipid peroxidation in liver and kidney were observed with NiCl2 dosages ranging from 0.12 to 0.75 mmol per kg, sc. Intrarenal administration of a carcinogenic nickel compound, nickel subsulfide (Ni3S2, 0.36 mmol per kg body wt), did not affect MDA concentrations in the injected kidneys of rats killed one to 20 days post-injection. The results of this study implicate lipid peroxidation as a molecular mechanism for cell injury in acute NiCl2 poisoning, but they do not furnish any evidence that lipid peroxidation is involved in the initiation of nickel carcinogenesis.

Animals↗
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Electrothermal atomic absorption spectrophotometry of nickel in tissue homogenates.

A method for analysis of Ni concentrations in tissues is described, which involves (a) tissue dissection with metal-free obsidian knives, (b) tissue homogenization in polyethylene bags by use of a "Stomacher" blender, (c) oxidative digestion with mixed nitric, sulfuric, and perchloric acids, and (d) quantitation of Ni by electrothermal atomic absorption spectrophotometry with Zeeman background correction. The detection limit for Ni in tissues is 10 ng per g, dry weight; the coefficient of variation ranges from 7 to 15 percent, depending on the tissue Ni concentration; the recovery of Ni added in concentration of 20 ng per g, dry weight, to kidney homogenates averages 101 +/- 8 percent (mean +/- SD). In control rats, Ni concentrations are highest in lung (102 +/- 39 ng per g, dry weight) and lowest in spleen (35 +/- 16 ng per g, dry wt.). In descending order of Ni concentrations, the tissues of control rats rank as follows: lung greater than heart greater than bone greater than kidney greater than brain greater than testis greater than fat greater than liver greater than spleen. In rats killed 24 h after sc injection of NiCl2 (0.125 mmol per kg, body weight) Ni concentrations are highest in kidney (17.7 +/- 2.5 micrograms per g, dry weight) and lowest in brain (0.38 +/- 0.14 micrograms per g, dry weight). In descending order of Ni concentrations, the tissues of NiCl2-treated rats rank as follows: kidney much greater than lung greater than spleen greater than testis greater than heart greater than fat greater than liver greater than bone greater than brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
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Blood nickel concentrations in patients with stainless-steel hip prostheses.

Nickel concentrations were analyzed by electrothermal atomic absorption spectrophotometry in serum and whole blood specimens from patients 9 to 15 years after unilateral (N = 11) or bilateral (N = 2) hip arthroplasty. The hip prostheses were of the "Charnley" or "TR-28" (metal-to-plastic) types, fabricated of stainless-steel (14 to 16 percent Ni) with polyethylene acetabular cups. In 12 of the 13 patients, nickel concentrations (+/- SD) averaged 0.30 +/- 0.25 microgram per L (range 0.05 to 0.85) in serum and 0.36 +/- 0.20 microgram per L (range 0.11 to 0.67) in whole blood; these values did not differ significantly from the corresponding nickel concentrations in specimens from 30 healthy controls (0.28 +/- 0.24 microgram per L, range less than 0.05 to 1.08, in serum; 0.34 +/- 0.28 microgram per L, range less than 0.05 to 1.05, in whole blood). The remaining patient, a 78-year-old man with bilateral hip arthroplasty, had nickel concentrations of 3.1 micrograms per L in serum and 2.3 micrograms per L in whole blood; renal insufficiency apparently contributed to hypernickelemia in this patient. The arthroplasty patients were asymptomatic with respect to their joint replacements; X-rays at the last follow-up examinations did not reveal bone resorption around the implants. This study shows that patients with stainless-steel hip prostheses of the metal-to-plastic types do not develop hypernickelemia in the apparent absence of corrosion, local complications, or systemic conditions, such as renal insufficiency.

Adult↗
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Serum ceruloplasmin concentrations in rats with primary and transplanted sarcomas induced by nickel subsulfide.

Ceruloplasmin (CPN) concentrations were measured by p-phenylenediamine oxidase assay in serums from (a) 30 control Fischer rats; (b) 5 rats with primary sarcomas induced by i.m. injection of nickel subsulfide (alpha Ni3S2), and (c) 12 rats at intervals up to six weeks after s.c. transplantation of four alpha Ni3S2-induced sarcomas. Serum CPN concentrations were not significantly increased in rats with primary sarcomas (mean = 0.38 g per liter) (S.D. +/- 0.05), versus 0.35 g per liter (S.D. +/- 0.04) in controls. In contrast, serum CPN concentrations were increased within 11 to 21 days in all rats with transplanted sarcomas. Maximum concentrations of serum CPN occurred at 31 to 34 days after tumor transplantation, (mean = 0.56 +/- 0.05 g per liter), equivalent to 1.6 +/- 0.2 times the initial CPN concentrations in serums obtained prior to treatment (P less than 0.001). The development of hyperceruloplasminemia in rats with transplanted sarcomas and not in rats with primary sarcomas is attributed to greatly enhanced growth-rates of the transplanted neoplasms.

Animals↗
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Use of teflon digestion bombs for tissue analysis: measurements of the effect of estradiol-17 beta upon hepatic copper in rats.

Teflon digestion bombs have been used for pressure decomposition of rat liver samples preliminary to copper analyses by atomic absorption spectrometry. The analytical procedure is convenient and is consistently free from copper contamination. The recovery of copper added to liver samples (three mug Cu added per g wet wt) averaged 102 (S.D. plus or minus 3) percent. The accuracy of the copper analyses was verified by use of National Bureau of Standards reference bovine liver. The mean concentration of copper in perfused livers of 16 untreated male rats averaged 16.1 (S.D. plus or minus 2.3) mug per g dry wt. The mean concentration of copper in perfused livers of 8 male rats which received estradiol-17 beta in dosage of 50 mug per day, s.c., for 21 consecutive days was 21.7 (S.D. plus or minus 4.7) mug per g dry wt (p vs controls equals greater than 0.01). This study demonstrates that estrogen administration can cause a significant increase in the concentration of hepatic copper.

Animals↗