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At least 217 records · Page 12Linked to original sources
PubMed1989

Testosterone as a factor modifying the toxicity of ekatin for the Pharaoh quail (Coturnix coturnix Pharaoh). I. Mature birds.

1. Testosterone reduces the haemolytic action of Ekatin on the morphotic blood elements by accelerating maturation of erythroblastic cells. 2. Testosterone, by accelerating the metabolism of the pesticide causes a defective defence processes of the organism by decreasing the number of macrophages. 3. Intoxication of androgenised birds with Ekatin leads to a breakdown of the systemic adaptive mechanisms by rapid and early switching on the adrenal cortex in response to the stress caused by poisoning.

Animals↗
PubMed1991

Stilbestrol as a factor modifying the toxicity of Ekatin for the Pharaoh quail (Coturnix coturnix Pharaoh). I. Young birds.

1. The noted fall of the erythrocyte count, haemoglobin and haematocrit levels after stilbestrol indicate that this hormone disturbs erythropoiesis, probably by depressing the maturation of erythroid cells in the bone marrow. 2. The reaction of the erythrocyte system of birds intoxicated with Ekatin indicates that this pesticide has a haemolytic influence on the morphotic elements of the blood. 3. Estrogenisation enhances the action of Ekatin on the erythrocyte system by as it seems increasing the susceptibility of the red blood cells to the haemolytic action of this pesticide. 4. The high heterophilic leucocytosis in birds receiving stilbestrol is evidence that this hormone causes by an increased release of corticoids, hyperplasia of the granulopoietic tissue in the bone marrow and depresses the marrow barrier for heterophils. 5. Changes in the leucocyte system of quails intoxicated with Ekatin indicate a stressogenic action of this poison. 6. The reaction of the latter system to Ekatin administered after estrogenisation seems to be an indication that stilbestrol reduces the susceptibility of the quails to the stressogenic action of the pesticide.

Animals↗
PubMedDate not supplied

Omega-3 fatty acids and selenium as coronary heart disease risk modifying factors in Asian Indian and Chinese males.

OBJECTIVE: Asian Indian men are reported to have a higher incidence of coronary heart disease than men of other ethnic groups worldwide. Among the many hypotheses, one possible risk factor may be related to their dietary habits. This study estimated the plasma concentrations of fatty acids, antioxidant vitamins, and selenium in Indians and Chinese of Singapore. METHODS: The study population consisted of 145 Indian men and 147 Chinese men ages 26 to 79 y from a cross-sectional survey, the National University of Singapore Heart Study. RESULTS: Our findings indicated that Indians had lower plasma concentrations of docosahexanoic acid (3.07% versus 3.54%, P < 0.001), alpha-linolenic acid (0.48% versus 0.57%, P < 0.001), and total omega-3 fatty acids (4.71% versus 5.27%, P < 0.001) than did the Chinese. Arachidonic acid was higher in Indians (4.83%) than in the Chinese (4.51%, P = 0.007). The ratio of omega-3 acid to omega-6 fatty acid was also lower in Indians (0.15) than in the Chinese (0.16, P = 0.007). There were no significant differences in the concentrations of monounsaturated fatty acids, but saturated fatty acids were higher in Indians (39.17%) than in the Chinese (38.28%, P < 0.001). Analysis of vitamins A, C, and E showed no significant differences between Indians (0.67, 5.72, and 13.04 mg/L, respectively) and Chinese (0.68, 6.48, and 12.71 mg/L, respectively); however, serum concentration of selenium in Indians (117.49 microg/L) was significantly lower than in the Chinese (126.72 microg/L, P < 0.001). CONCLUSION: The results suggest that lower plasma concentrations of omega-3 fatty acids and selenium and higher concentrations of arachidonic acid and saturated fatty acids in Indians may reflect lower intakes of marine foods and, as a consequence, higher susceptibility to coronary heart disease.

Adult↗
PubMed1986

Generation and dose as modifying factors of inorganic mercury accumulation in brain, liver, and kidneys of rats fed methylmercury.

Through three generations, male rats were fed a commercial chow supplemented with four levels of methyl mercury; the average mercury concentrations were 0.038, 0.18, 7.23, and 33.92 nmol Hg/g food for control, low, middle, and high dose groups, respectively. No clinical abnormalities except enlarged kidneys were found in these animals. The effects of dose and generation on tissue distribution and accumulation of inorganic mercury and total mercury were studied in the brain, kidneys, and liver. The dose level of methyl mercury greatly determined the organ accumulation of total mercury and inorganic mercury, as well as the ratio of inorganic mercury concentration to total mercury concentration (I/T) in organs. The I/T ratio was inversely related to the dose level of methyl mercury. With generational procession, the most notable change was found in the liver, i.e., the increasing I/T ratio and the decreasing total mercury accumulation at any dose level. In contrast, the I/T ratio in the kidney showed no constant tendency with generation. The present results suggest that the generational enhancement of inorganic mercury formation from methyl mercury occurs mainly in the liver.

Animals↗
PubMed1999

4-Hydroxynonenal as a second messenger of free radicals and growth modifying factor.

Immunohistochemical analysis of the distribution of the lipid peroxidation product 4-hydroxynonenal (HNE) in the brain of baboons exposed to experimental hemorrhagic traumatic shock or sepsis showed that systemic oxidative stress and the thereby generated HNE affect the blood:brain barrier and the regulation of cerebral blood flow determining secondary brain damage. Similarly, HNE was determined during ischemia in the brain blood vessels of rats exposed to ischemia/reperfusion injury of the brain. After reperfusion, HNE disappeared from the blood vessels but remained in neurones and in glial cells. Since HNE modulates cell proliferation and differentiation (including proto-oncogene expression), it is postulated that HNE might have prominent local and systemic effects that are not only harmful but beneficial, too, determining the outcome of various pathophysiological conditions based on oxidative stress.

Aldehydes↗
PubMed2002

Dichloroacetate toxicokinetics and disruption of tyrosine catabolism in B6C3F1 mice: dose-response relationships and age as a modifying factor.

Dichloroacetate (DCA) is a rodent carcinogen commonly found in municipal drinking water supplies. Toxicokinetic studies have established that elimination of DCA is controlled by liver metabolism, which occurs by the cytosolic enzyme glutathione-S-transferase-zeta (GST-zeta). DCA is also a mechanism based inhibitor of GST-zeta, and a loss in GST-zeta enzyme activity occurs following repeated doses or prolonged drinking water exposures. GST-zeta is identical to an enzyme that is part of the tyrosine catabolism pathway known as maleylacetoacetate isomerase (MAAI). In this pathway, GST-zeta plays a critical role in catalyzing the isomerization of maleylacetoacetate to fumarylacetoacetate. Disruption of tyrosine catabolism has been linked to increased cancer risk in humans. We studied the elimination of i.v. doses of DCA to young (10 week) and aged (60 week) mice previously treated with DCA in their drinking water for 2 and 56 weeks, respectively. The diurnal change in blood concentrations of DCA was also monitored in mice exposed to three different drinking water concentrations of DCA (2.0, 0.5 and 0.05 g/l). Additional experiments measured the in vitro metabolism of DCA in liver homogenates prepared from treated mice given various recovery times following treatment. The MAAI activity was also measured in liver cytosol obtained from treated mice. Results indicated young mice were the most sensitive to changes in DCA elimination after drinking water treatment. The in vitro metabolism of DCA was decreased at all treatment rates. Partial restoration ( approximately 65% of controls) of DCA elimination capacity and hepatic GST-zeta activity occurred after 48 h recovery from 14 d 2.0 g/l DCA drinking water treatments. Recovery from treatments could be blocked by interruption of protein synthesis with actinomycin D. MAAI activity was reduced over 80% in liver cytosol from 10-week-old mice. However, MAAI was unaffected in 60-week-old mice. These results indicate that in young mice, inactivation and re-synthesis of GST-zeta is a highly dynamic process and that exogenous factors that deplete or reduce GST-zeta levels will decrease DCA elimination and may increase the carcinogenic potency of DCA. As mice age, the elimination capacity for DCA is less affected by reduced liver metabolism and mice appear to develop some toxicokinetic adaptation(s) to allow elimination of DCA at rates comparable to naive animals. Reduced MAAI activity alone is unlikely to be the carcinogenic mode of action for DCA and may in fact, only be important during the early stages of DCA exposure.

Administration, Oral↗
PubMed1999

Hypothesis: is low prenatal vitamin D a risk-modifying factor for schizophrenia?

The central nervous system is increasingly being recognised as a target organ for vitamin D via its wide-ranging steroid hormonal effects and via the induction of various proteins such as nerve growth factor. This paper proposes that low maternal vitamin D may impact adversely on the developing foetal brain, leaving the affected offspring at increased risk of adult-onset schizophrenia. The hypothesis can parsimoniously explain diverse epidemiological features of schizophrenia, such as the excess of winter births, increased rates of schizophrenia in dark-skinned migrants to cold climates, the increased rate of schizophrenia births in urban versus rural setting, and the association between prenatal famine and schizophrenia. Studies that will allow rejection of the hypothesis are proposed.

Adult↗
PubMed2001

BAPS prize-1999: Lung growth induced by prenatal tracheal occlusion and its modifying factors: a study in the rat model of congenital diaphragmatic hernia.

BACKGROUND/PURPOSE: Prenatal tracheal occlusion (TO) has been shown to accelerate lung growth in animal models and models of pulmonary hypoplasia. However, these models may not mimic early events in human congenital diaphragmatic hernia (CDH). The authors previously have developed a model of TO in the rat. The purpose of this study was to apply this technique to characterize TO-induced lung growth in the early onset nitrofen-induced model of CDH, and to address the clinically important questions of the effect of timing of TO and maternal infusion of terbutaline on TO-induced lung growth. METHODS: Left-sided CDH was induced in the fetuses of time-dated pregnant Sprague-Dawley rats by feeding 100 mg of nitrofen on day 9 of gestation. TO was performed via maternal laparotomy and hysterotomy at 19 days' gestation. At harvest (21.5 days' gestation), lungs from nitrofen-exposed fetuses without CDH (non-CDH), with CDH (CDH), and with CDH and TO (CDH-TO) were compared by analysis of wet and dry weight, DNA and protein content, and stereologic morphometry. A second study was performed to assess relative lung growth achieved by equal intervals of TO after "early" (19 days) versus "late" (20 days) gestational TO. Finally, the effect of maternal infusion of terbutaline, a commonly used tocolytic for fetal surgery, on TO-induced lung growth was analyzed. RESULTS: Analysis of lung growth showed consistent and significant lung growth in CDH-TO lungs. Lung growth after TO was proliferative and characterized by an increase in parenchymal volume as manifest by increased total saccular number and surface area and radial saccular count. Although visceral reduction was partially achieved, herniated liver was reduced incompletely. The majority of lung growth occurred during the latter half of the TO period. Early gestational age at TO and maternal terbutaline administration adversely influenced lung growth in CDH-TO fetuses. CONCLUSIONS: Prenatal TO induces dramatic lung growth in the early onset, nitrofen-induced rat model of CDH. TO is more effective later in gestation presumably because of the advanced stage of lung development and lung fluid production. This effect could be counterbalanced by the use of beta-mimetic tocolytic, which inhibits fetal lung fluid production late in gestation. Multiple factors including fetal lung fluid production and absorption, pharmacologic agents, space-occupying herniated viscera, and timing and duration of TO may be important clinical variables. The development of the rat model should facilitate further studies into the cellular and molecular mechanisms responsible for TO-induced lung growth.

Animals↗
PubMed2002

The 99 and 170 loop-modified factor VIIa mutants show enhanced catalytic activity without tissue factor.

To elucidate the functions of the surface loops of VIIa, we prepared two mutants, VII-30 and VII-39. The VII-30 mutant had all of the residues in the 99 loop replaced with those of trypsin. In the VII-39 mutant, both the 99 and 170 loops were replaced with those of trypsin. The k(cat)/K(m) value for hydrolysis of the chromogenic peptidyl substrate S-2288 by VIIa-30 (103 mm(-)1s(-)1) was 3-fold higher than that of wild-type VIIa (30.3 mm(-)1 s(-)1) in the presence of soluble tissue factor (sTF). This enhancement was due to a decrease in the K(m) value but not to an increase in the k(cat) value. On the other hand, the k(cat)/K(m) value for S-2288 hydrolysis by VIIa-39 (17.9 mm(-)1 s(-)1) was 18-fold higher than that of wild-type (1.0 mm(-)1 s(-)1) in the absence of sTF, and the value was almost the same as that of wild-type measured in the presence of sTF. This enhancement was due to not only a decrease in the K(m) value but also to an increase in the k(cat) value. These results were in good agreement with their susceptibilities to a subsite 1-directed serine protease inhibitor. In our previous paper (Soejima, K., Mizuguchi, J., Yuguchi, M., Nakagaki, T., Higashi, S., and Iwanaga, S. (2001) J. Biol. Chem. 276, 17229-17235), the replacement of the 170 loop of VIIa with that of trypsin induced a 10-fold enhancement of the k(cat) value for S-2288 hydrolysis as compared with that of wild-type VIIa in the absence of sTF. These results suggested that the 99 and the 170 loop structures of VIIa independently affect the K(m) and k(cat) values, respectively. Furthermore, we studied the effect of mutations on proteolytic activity toward S-alkylated lysozyme as a macromolecular substrate and the activation of natural macromolecular substrate factor X.

Amino Acid Sequence↗