Reaction and disruption for Fe/La1.85Sr
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Biomedical subjects
Publications and source records attributed to Y Gao.
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We tested the hypothesis that atrial natriuretic factor (ANF) may play a role in the development of hypertension in salt-sensitive Dahl (S) rats as compared to normotensive salt-resistant Dahl (R) rats. We measured immunoreactive ANF in plasma and atria of the inbred (JR) strain of Dahl S and R rats receiving 0.9 or 8% NaCl diets for up to 8 weeks. We also tested the effect of acute volume expansion on plasma and atrial ANF values in rats receiving the 0.9% salt diet. In addition, we examined the effects of exogenous ANF in the form of atriopeptin III given as intravenous bolus infusion at both levels of salt intake. We found no difference in plasma and atrial values between S and R rats irrespective of salt intake. The S and R rats showed a similar, five- to sevenfold increase of plasma ANF in response to acute saline expansion. Finally, we were unable to demonstrate differences between S and R rats in response to atriopeptin III with respect to transient decreases in blood pressure, and pronounced increases in glomerular filtration rate (GFR), renal blood flow or natriuresis. These results do not reveal appreciable changes in the ANF system of Dahl S rats either before or after onset of hypertension when compared to normotensive R rats. Therefore, our findings do not support the notion that ANF is important in the development or maintenance of chronic salt-induced hypertension in S rats.
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In Linxian County, a high incidence area of esophageal cancer, staple food is heavily contaminated by fungi of Fusarium genus. In this paper, it is demonstrated for the first time that T-2 toxin produced by Fusarium can induce various structural aberrations in chromosomes of cultured human peripheral lymphocytes. Peripheral blood cells from 10 normal subjects were cultured for 48 hours. 8732 metaphase plates were analysed, including T-2 toxin-treated group and the control group. The average rate of chromosome aberration was 6.88% in the toxin group, while only 0.2% in the control group. There was a significant difference between these two groups (P less than 0.001). It was observed that T-2 toxin had both mitogenic and direct cytotoxic effects on human lymphocytes. At a lower dose of T-2 toxin (0.1-5 ng/ml for 24 hours), the number of mitosis was increased and chromosome aberration was induced but at a higher dose (10-100 ng/ml), T-2 toxin inhibited mitosis and killed the cells. These results suggest that T-2 toxin possess a carcinogenic potential.
Studies were carried out to compare the 5'-deiodination reactions of thyroxine (T4) and 3,3'-5'-triiodothyronine (rT3) in 2.5% rat liver homogenates. The 5'-deiodinase activity was assayed by the 3,5,3'-triiodothyronine (T3) produced from T4 or by 125I-rT3. Under our experimental conditions, the two 5'-monodeiodination reactions resulted in similar apparent KMs: 1.5 microM for T4 and 1.1 microM for rT3. However, the apparent Vmax values of T4 and rT3 deiodination reactions were, respectively, 0.91 and 222 pmol/mg protein/min. Both reactions were stimulated by thiol reagents but only rT3 deiodination showed complete thiol dependence. The inhibitory effect of 6-propyl-2-thiouracil on the 5'-deiodination of rT3 was at least 50 fold greater than that of T4. The divalent ion requirement of the deiodination system was tested with CaCl2, MgCl2, and ZnCl2 at a range of concentrations. Zinc ion appeared to be a potent inhibitor in both T4 and rT3 deiodination systems. Only the 5'-deiodination of rT3 was inhibited slightly by low concentrations of calcium and magnesium ions. Our results suggest that based on their apparently distinct regulation mechanisms, the 5'-monodiodination of T4 and rT3 in rat liver homogenates is likely mediated by more than one enzyme, despite the similarity of observed KMs.
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T-2 toxin is an important representative of trichothecenes produced by various species of imperfect fungi, mainly Fusarium genus. It is a naturally occurring toxin that can cause severe diseases in human and animals. No definite data demonstrating the carcinogenic potential of T-2 toxin had been reported up to now. We demonstrated that T-2 toxin reproducibly induced chromosomal structural aberrations both in cultured human peripheral blood lymphocytes as well as in V79 Chinese hamster fibroblasts. The mean percentage of cells with aberration of human lymphocytes from normal individuals induced by T-2 toxin is 49-fold (9.8%) of the mean percentage of corresponding control cultures without T-2 toxin (0.2%). T-2 toxin induced chromosome type (76%) as well as chromatid type (24%) of aberrations; among them, acentric fragment (46%) was the most common type, and chromatid gap, deletion, and chromosome gap were the next most common. T-2 toxin can induce aberrations in cells at different phases of the cell cycle. There are definite dose-effect relationships within a certain range of dosage of T-2 toxin in experiments with both human peripheral blood lymphocytes and V79 cells. T-2 toxin exhibited three types of effects on cells, namely, mitogenic at lowest concentration, clastogenic (chromosome aberration) at median concentration, and cytotoxic at higher concentration. The dose-effect curves of these three effects are partly overlapping. There is some interindividual difference in sensitivity of response for the clastogenic effect of T-2 toxin, but no resistant individual was observed. Sex or age effect was not observed. The above results suggest that T-2 toxin has carcinogenic potentials. The dosage of aflatoxin that can induce chromosomal aberration of human peripheral blood lymphocytes is thousands-fold of the dosage of T-2 toxin as shown in this report. T-2 toxin might have more hazardous potentials than had been previously considered. The carcinogenic potential of T-2 toxin and related trichothecenes and their possible roles in carcinogenesis of upper gastrointestinal (G.I.) tract cancers need to be further investigated.
To examine the physiological role of atrial natriuretic factor (ANF) in the maintenance of sodium homeostasis under various conditions, we performed experiments in rats across a wide range of sodium intake, in rats with chronic renal insufficiency at extremes of sodium intake, and in rats given desoxycorticosterone acetate. After three weeks of a very low sodium diet, regular diet, or regular diet plus 1% saline as drinking water, no difference in plasma values of immunoreactive atrial natriuretic factor (IR-ANF) were identified, while rats at the lowest level of sodium intake had elevated atrial values. Normal rats, and rats with 5/6 nephrectomy has plasma values of IR-ANF which were no different irrespective of their sodium intake, nor were atrial values in these rats different. Although mineralocorticoid "escape" could be documented by changes in urine sodium excretion, neither plasma nor atrial IR-ANF values showed differences either at 24 or 72 hr after "escape". The data are consistent with previous observations that ANF serves the purpose of affecting rapid adjustments to large alterations in circulating fluid volume. Chronic high sodium intake, adaptation to renal insufficiency, and adjustment to the effect of mineralocorticoid do not appear to be associated with increased circulating plasma concentrations of IR-ANF.
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