Ribonucleic acid biosynthesis in methylcholanthrene-treated rats.
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Animals↗
Biomedical subjects
J A Knight
Publications and source records attributed to J A Knight.
The impact of confrontation in learning.
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Achievement↗
The psychological care of the allergic patient.
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Chronic Disease↗
The liaison psychiatrist in kidney transplantation.
Medical progress in transplantation has given rise to special psychiatric problems requiring understanding and proper care. If these problems are to be adequately addressed, psychological services should be available in all activities of the transplant unit. This paper discusses the role of the consultation liaison psychiatrist with patients and colleagues in kidney transplantation. Areas for exploration in evaluating prospective donors and recipients are identified. While body image problems emerge infrequently in kidney transplantation, careful psychological screening may identify some of these potential difficulties and set the stage for dealing with them. The discussion of pertinent issues and possible complications with patients proves to be an effective, preventive approach. While most members of a transplant team are aware of the ethical dimensions in transplantation, psychiatrists, by the very nature of their work as students of human behavior, are pulled directly into these issues. Further, the atmosphere on the transplant unit should be constantly monitored in order to nurture a healing environment for both patients and staff.
Body Image↗
Menetrier's disease in children: report of a case and review of the pediatric literature.
A case of Menetrier's disease (giant hyperplasia of the gastric mucosa) in a 2-day-old infant is presented. The lesion was primarily confined to the gastric antrum. It resulted in outlet obstruction and necessitated partial gastrectomy. The pertinent literature is critically evaluated, and probably only 2 of the 9 previously reported cases of Menetrier's disease in children qualify fully.
Female↗
The effect of metal chelators on lipid peroxidation in irradiated erythrocytes.
Prophylactic irradiation of blood and blood components is accepted practice in order to prevent graft-versus-host disease from infused lymphocytes. Irradiation, however, results in increased red cell potassium (K+) loss, along with other possible effects that may affect red cell function and viability. Lipid peroxidation (LP), a process initiated by the production of oxygen free radicals, is increased in red cells in the presence of reactive iron species and various heme moieties. In this report, it is noted that not only is plasma K+ significantly increased following blood irradiation, but LP is also increased compared with paired non-irradiated blood samples. Furthermore, various metal chelators significantly reduce LP in the irradiated samples. These chelators also significantly reduced the rate of cellular K+ loss during the four day 37 degrees C incubation period. This study further suggests that the addition of selected metal chelators may be effective in both irradiated and non-irradiated stored blood by improving the function and viability of transfused erythrocytes.
Chelating Agents↗
The effect of metal chelators on lipid peroxidation in stored erythrocytes.
Lipid peroxidation, an autocatalytic free radical process, is increased in a wide variety of conditions including various hemolytic anemias and hemoglobin disorders. Increased erythrocyte lipid peroxidation occurs in the presence of iron species and some heme moieties. In this study, greatly reduced concentrations of malondialdehyde (MDA), an indicator of lipid peroxidation, were observed in stored blood anticoagulated with citrate, phosphate, dextrose, and adenine (CPDA-1) upon the addition of deferoxamine mesylate (DM), diethylenetriaminepentaacetic acid (DTPA), and ethylenediaminetetraacetic acid (EDTA) (P less than 0.001). Human transferrin has essentially no effect on lipid peroxidation. Conversely, penicillamine and butylated hydroxytoluene significantly increased lipoperoxide production. Although bathophenanthroline disulfonic acid (BPD) appeared to be very effective in reducing lipid peroxidation, its complex chromatographic patterns which were due to the presence of multiple thiobarbituric acid reactive substances, were difficult to fully evaluate. The addition of appropriate metal chelators to stored blood may be effective in increasing the viability and longevity of transfused red cells.
Anticoagulants↗
Pathological reactions in lung, liver, thymus, and spleen of rats after subacute parenteral administration of nickel sulfate.
Male Fischer-344 rats (10 to 12 rats per group) were given 14 i.m. injection of nickel sulfate (NiSO4) over a period of 26 days in order to delineate the two-year survival, body weight curves, hematocrit responses, and histopathological reactions, including carcinogenesis. Group A (vehicle controls) received the NaCl vehicle; Groups B, C, and D received NiSO4 solution at dosages of 63, 83, or 125 mumol per kg, respectively. Rats in Group D all died during the period from 4 to 32 days after the first injection; survival of rats in Groups B and C did not differ significantly from the controls (Group A). No differences were found at any time between the mean body weights or blood hematocrits of the NiSO4-treated groups vs. the controls. In Group D, histopathological lesions of the lung, liver, thymus, and spleen were consistently observed; these lesions were most severe in rats that died during the period from 22 to 32 days after the first injection. The lungs showed proliferation of alveolar lining cells, thickening of the alveolar wall, and proteinaceous alveolar exudate. The livers showed microvesicular steatosis, and necrotic hepatocytes were scattered throughout the lobules. Degeneration of lymphocytes, with pyknosis and karyorrhexis, was observed in the thymic cortex and the white pulp of the spleen. At necropsy, no significant differences were found between the NiSO4-treated rats of Groups B and C and the controls (Group A). No sarcomas or other neoplasms occurred near the injection sites in NiSO4-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Peroxidation of linolenic acid--catalysis by transition metal ions.
Numerous studies have demonstrated that several indices of oxidative damage are enhanced in target tissues of rodents exposed to various transition metal ions. Whether or not these indices represent primary or secondary effects are not known, since tissues injured by other mechanisms are susceptible to an increased rate of lipid peroxidation (LP). In the current study, the reaction mixtures (metal ions with linolenic acid) were preincubated at 37 degrees C for 24 hours prior to the measurement of malondialdehyde (MDA) by liquid chromatography, and conjugated dienes at 233 nm. These metal-catalyzed reactions were also compared in the presence of butylated hydroxytoluene (BHT), a free radical scavenger. Our results showed that Cd(II), Co(II), Cu(II), Fe(II & III), Mn(II), and Ni(II) all significantly increased the concentration of MDA and conjugated dienes over LA controls (P less than 0.001 by Mann-Whitney test). The production of MDA and conjugated dienes was also increased by Al(III) but to a lesser degree (P less than 0.05 and 0.01, respectively); As(V) did not increase either index. The addition of butylated hydroxytoluene (BHT) to the reaction mixtures significantly reduced the production of MDA (P less than 0.001). These in vitro studies support prior in vivo reports that the primary mechanism of the acute toxic effects of these metal ions is due, at least in part, to metal-catalyzed peroxidation of polyunsaturated fatty acids.
Butylated Hydroxytoluene↗
Nickel inhibition of the osmotic-sensitive ionic cellular channels.
The effects of nickel on cell volume regulation were studied in isolated proximal renal tubules from Carassius auratus (goldfish). Variations in cell volume were measured as changes in the external tubular diameters as a function of time of exposure to NiCl2 (Ni(II] in both isotonic and hypotonic solutions. Renal tubules were first incubated in isotonic fish Ringer's solution (290 mOsm) with and without 0.05, 0.10, 0.50, and 1.00 mmol/L Ni(II) for three minutes. After this period, the bath solution was rapidly changed to hypotonic NaCl-poor Ringer's solution (110 mOsm). Renal cells exposed to Ni(II) (0.05 to 1.00 mmol/per L) did not undergo cell swelling in isotonic solutions. However, in a dose related manner, Ni(II) inhibited the volume regulatory process of cells exposed to hypotonic solutions. The effect of Ni(II) on cell volume regulation was specific to the osmoregulatory phase; that is, while there was no inhibition of the hypotonically-induced cell swelling (osmometric phase), there was a significant dose-dependent inhibition of the cellular volume regulatory decrease that follows (osmoregulatory phase). It is postulated by us that nickel inhibition of the osmoregulatory process is secondary to an inhibition of the osmotic sensitive ionic channels.
Animals↗
Increased urinary lipoperoxide levels in renal transplant patients.
Using high performance liquid chromatographic methods, both plasma and urine lipoperoxide concentrations were measured, as malondialdehyde (MDA), in 30 stable renal transplant patients receiving daily cyclosporine and/or azathioprine therapy. Their MDA concentrations were compared with previously reported reliable reference values using the same liquid chromatographic methods. Although their plasma concentrations were within the reference range, their mean urine MDA values averaged 3.7 to 5.0 times the normal reference values (p less than 0.001). The primary cause of the increased urine MDA concentrations following renal transplantation in these patients is unknown; it could be due to (a) renal lipid peroxidation directly related to the cyclosporine/azathioprine therapy, (b) drug-induced or other nephrotoxicity by an alternative mechanism with secondary lipid peroxidation, (c) increased lipid peroxidation owing to an immunologic response to the kidney graft, or (d) a combination of these possibilities.
Azathioprine↗
Metal-catalyzed peroxidation of polyunsaturated fatty acids.
In this study malondialdehyde (MDA) was measured as the thiobarbituric acid (TBA) adduct by high performance liquid chromatography with linolenic acid (LA), as well as with LA to which the following metal ions were added: Ag+1, Al+3, As+5, Ba+2, Cd+2, Co+2, Cu+1, Cu+2, Fe+2, Fe+3, Hg+2, Mn+2, Ni+2, Pb+2, and Zn+2. Our results showed that Fe+3 is a particularly potent catalyst of this oxidation reaction. Several other metals also significantly increased the production of MDA over LA alone, as shown by the Mann-Whitney test, including Al+3 and Fe+2 (p less than 0.001), Cu+2, Ba+2, Mn+2 (p less than 0.01), and As+5 (p less than 0.05). Pb+2 almost completely inhibited the production of MDA from LA (p less than 0.001). Addition of the free radical scavenger, butylated hydroxytoluene (BHT), significantly inhibited MDA formation in these latter reactions, indicating they are free-radical mediated. Pre-incubation of the reaction mixtures at 37 degrees C and physiologic pH with both Fe+2 and Fe+3 greatly increased MDA formation, suggesting that in acute metal toxicity the initiating free-radical process might be primarily due to direct metal catalysis of preformed lipid peroxides.
Butylated Hydroxytoluene↗
Increased urinary lipoperoxides in drug abusers.
Urine lipoperoxides were measured, as the malondialdehyde-thiobarbituric acid adduct, by "high performance" liquid chromatography in men who tested positive for any of the common "drugs of abuse." Urine malondialdehyde concentrations were within the reference range in those urines containing barbiturates and amphetamines. On the other hand, significant urine malondialdehyde elevations were associated with those testing positive for marijuana (p less than 0.005), cocaine, opiates, benzodiazepines, and in those urines containing multiple drugs (p less than 0.001). The mechanism of tissue damage by these drugs is not necessarily by lipid peroxidation, since their primary toxic effects might result in cellular injury by an alternative mechanism; the observed increased lipid peroxidation could be a secondary phenomenon following tissue injury.
Amphetamine↗
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↗
Serial lactic dehydrogenase and glutamic oxaloacetic transaminase automated analysis.
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Aspartate Aminotransferases↗
The process and theories of aging.
A wide variety of theories to explain the aging process have been proposed including: (1) stochastic (somatic mutation, error catastrophe, protein glycosylation); (2) developmental (immune and neuroendocrine); (3) programmed (genome-based); and (4) free radical. Although no single hypothesis fully explains all aging phenomena, the genome-based and free radical theories, in particular, are supported by significant observational and experimental evidence. In addition, these two proposals are related to each other in some respects, and possibly to other theories as well. Continued basic and clinical research in this highly complex and critically important area will add to our understanding and appreciation of the theoretical and practical implications of the aging process.
Aging↗
Diseases related to oxygen-derived free radicals.
Oxygen-derived free radicals are very important mediators of cell injury and death. Not only are these highly reactive chemical species important in the aging process, but they are either directly or indirectly involved in a wide variety of clinical disorders, such as atherosclerosis, reperfusion injury, pulmonary toxicity, macular degeneration, cataractogenesis, and cancer. In addition, they play an important role in chronic granulomatous disease and act as secondary sources of cellular injury in chronic granulomatous disease and act as secondary sources of cellular injury in chronic inflammatory processes and several disorders of the central nervous system. Furthermore, a wide variety of drugs and xenobiotics are themselves either converted to, or stimulate the formation of, free radicals. Prevention and/or treatment of many of these disorders may be possible by appropriate antioxidant therapy, either currently available or to be discovered through continued research.
Disease↗
The effects of various antioxidants on lipid peroxidation in stored whole blood.
Since the introduction of acid-citrate-dextrose (ACD) in 1947 to anticoagulate and preserve whole blood for transfusion, various other improved nutrient formulas have been introduced that have significantly increased the viability and lifespan of stored erythrocytes. More recently, several studies involving lipid peroxidation have been reported in an attempt to understand alternative mechanisms that might lead to a further increase in red cell viability and extend the storage life of whole blood. In the current study, the effects of a variety of substances are reported whose antioxidant mechanisms differ; they include the transition metals manganese and zinc, the metal chelator phytic acid, and the free radical scavengers N-acetylcysteine, mannitol, uric acid, 1,3 dimethyluric acid, and quercetin. All but N-acetylcysteine, uric acid, and phytic acid were consistently effective in decreasing lipid peroxidation in stored red cells.
Antioxidants↗