Biomedical subjects

M C Reid

Publications and source records attributed to M C Reid.

42 records · Page 3Linked to original sources

PubMedDate not supplied

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↗

PubMedDate not supplied

Studies of the pathogenesis of arteriosclerosis induced in rats by intrarenal injection of a carcinogen, nickel subsulfide.

Widespread arteriosclerotic lesions were detected by histological examinations of rats killed at seven or nine weeks after an intrarenal (ir) injection of nickel subsulfide (Ni3S2, 5 mg per rat). Arteriosclerotic plaques were readily visualized by administering hematoporphyrin derivative (HPD) iv to rats at 24 hours before sacrifice. At necropsy, the major arteries were inspected under ultraviolet light, revealing patches of intense HPD-fluorescence in the arterial endothelium of Ni3S2-treated rats, but not in control rats. Consistent with previous reports, the Ni3S2-treated rats developed pronounced erythrocytosis; blood hematocrit values averaged 70 +/- 4 percent at seven weeks after ir injection of Ni3S2 (P less than 0.001 vs corresponding value of 49 +/- 2 percent in vehicle controls). At seven weeks, blood platelet counts averaged 17 percent lower and serum glucose concentrations averaged 23 percent lower in Ni3S2-treated rats than in controls; serum lipids, lipoproteins, non-protein nitrogen constituents, electrolytes, proteins, and enzymes were not significantly affected. Body weights and systolic blood pressures of rats at two, four, and six weeks after ir injection of Ni3S2 did not differ from corresponding values in controls. Addition of egg yolk to the diet caused mild hypercholesterolemia, but it did not enhance the incidence or severity of arterial lesions in Ni3S2-treated rats. These findings exclude hypertension and hyperlipidemia as pathogenic factors in Ni3S2-induced arteriosclerosis.

Animals↗

PubMedDate not supplied

Erythropoietin-mediated erythrocytosis in rodents after intrarenal injection of nickel subsulfide.

Rats and guinea pigs developed pronounced erythrocytosis at one to four months after unilateral intrarenal (ir) injection of nickel subsulfide (Ni3S2). For example, at two months after ir administration of Ni3S2 (5 mg) to rats, blood hematocrit values averaged 70 +/- 3 percent (p less than 0.001 vs. 48 4/- 2 in controls); at two months after ir administration of Ni3S2 (20 mg) to guniea pigs, blood hematocrit values averaged 67 +/- 6 percent (p less than 0.001 vs. 49 +/- 1 percent in controls). Hamsters and gerbils did not develop erythrocytosis after ir injection of Ni3S2 (5 mg/animal). Administration of Ni3S2 to rats by intrasplenic injection did not increase blood hematocrit; splenectomy did not prevent erythrocytosis in rats that received ir injection of Ni3S2. Erythrocytosis in rats was completely blocked by excision of the Ni3S2-injected kidney but was unaffected by excision of the non-injected kidney. Partial inhibition of Ni3S2-induced erythrocytosis in rats occurred after simultaneous ir injection of Mn, Cu, or Al dusts, benzo(a)pyrene, or subcutaneous (sc) infusion of sodium diethyldithiocarbamate. Erythrocytosis induced by ir injection of Ni3S2 was augmented by ir injection of Cr dust or intramuscular (im) administration of iron-dextran. Erythrocytosis occurred in rats after ir implantation of Ni3S2 within semi-permeable cellulose tubules, indicating that phagocytosis of Ni3S2 particles is unnecessary for erythropoietic stimulation. Erythropoietin (Ep) activity in rat serum increased sixfold at two weeks after ir injection of Ni3S2 (p less than 0.001 vs. controls), but Ep activity in pooled extracts of Ni3S2-treated rat kidneys did not increase significantly. This study identifies several factors that influence erythropoietic stimulation by Ni3S2, and furnishes salient information concerning the pathogenesis of Ni3S2-induced erythrocytosis.

Animals↗

PubMedDate not supplied

Rapid analysis of nickel in serum and whole blood by electrothermal atomic absorption spectrophotometry.

A method is described for analysis of nickel in serum and heparinized blood. After the sample has been subjected to protein precipitation with nitric acid and heat, nickel in the protein-free extract is measured by electrothermal atomic absorption with Zeeman background correction. The method is more sensitive, rapid, and convenient than previous techniques, and less subject to nickel contamination. Nickel concentrations in serums from New Zealand rabbits (mean +/- SD) average 4.0 +/- 2.5 micrograms per L, range = 0.9 to 11.9, N = 30; these results agree with measurements by the International Union of Pure and Applied Chemistry (IUPAC) reference procedure ( corr . coef . = 0.98). The following values are reported for nickel concentrations in serum and whole blood from healthy adult persons living in central Connecticut: serum, 0.46 +/- 0.26 micrograms per L, range = 0.1 to 1.3, N = 39; whole blood, 1.26 +/- 0.33 micrograms per L, range = 0.6 to 1.8, N = 30. This method is suitable for routine use in clinical and industrial laboratories.

Adult↗

PubMedDate not supplied

Effects of cobalt chloride, nickel chloride, and nickel subsulfide upon erythropoiesis in rats.

The erythropoietic effects of sustained intraperitoneal (i.p.) administration of CoCl2 and NiCl2 were compared with the effects of a single intrarenal (i.r.) injection of alpha Ni3S2 in female Fischer-344 rats. Infusion of NiCl2 by osmotic minipumps (0.85 mg Ni per day, i.p., for 24 days; total dose = 20 mg Ni per rat) did not alter the blood hematocrit or reticulocyte count during six weeks of observation. Under identical conditions, i.p. infusion of CoCl2 (0.85 mg Co per day, i.p., for 24 days; total dose = 20 mg Co per rat) caused significant erythrocytosis (hematocrit at six weeks = 62 +/- 4 percent, P less than 0.001 versus 50 +/- 3 percent in controls) and reticulocytosis (reticulocyte count at three weeks = 2.5 +/- 1.5 percent, P less than 0.005 versus 0.8 +/- 0.7 percent in controls). Administration of alpha Ni3S2 to rats as a single i.r. injection (7 mg Ni per rat) caused pronounced erythrocytosis (hematocrit at six weeks = 79 +/- 2 percent, P less than 0.001 versus controls) and reticulocytosis (reticulocyte count at three weeks = 2.8 +/- 1.2 percent, P less than 0.005 versus controls). This study demonstrates that i.p. infusion of Ni[II] is ineffective in stimulating erythropoiesis in rats, and that salient differences exist between the enhanced erythropoiesis that occurs in rats following i.p. infusion of Co[II] and that produced by i.r. injection of alpha Ni3S2.

Animals↗

PubMedDate not supplied

Use of methodological standards in diagnostic test research. Getting better but still not good.

OBJECTIVE: To determine the frequency and temporal changes in application of seven accepted methodological standards for the evaluation of diagnostic tests. DATA SOURCES: A search of the MEDLINE database yielded 1302 articles about diagnostic test studies, during a 16-year secular interval, 1978 through 1993, in four prominent general medical journals. STUDY SELECTION: In the 112 eligible studies, the test was intended for clinical use, indexes of accuracy (sensitivity and specificity or likelihood ratios) were provided, and more than 10 patients were enrolled. DATA EXTRACTION: Although each study was critically reviewed by one primary observer, a subset was independently evaluated for interrater consistency. DATA SYNTHESIS: The percentage of studies that fulfilled criteria for each of the seven methodological standards are as follows: (1) specify spectrum of evaluated patients, 27%; (2) report test indexes for clinical subgroups, 8%; (3) avoid workup bias, 46%; (4) avoid review bias, 38%; (5) provide numerical precision for test indexes, 11%; (6) report frequency and management of indeterminate results when calculating test indexes, 22%; and (7) specify test reproducibility, 23%. Secular increases were found for six of the seven standards in ranges of use from 14% to 31% during 1978-1981 to 1990-1993. Nevertheless, only one standard, avoidance of workup bias, was fulfilled by more than 50% of studies in the most recent secular interval. CONCLUSIONS: These results indicate that most diagnostic tests are still inadequately appraised. The routine demand for methodological standards could raise the quality of diagnostic test information, and the careful predissemination evaluation of diagnostic tests could eliminate useless tests before they receive widespread application.

Bias↗