scholarly journals Birthweight Depression in Male Rats Contiguous to Male Siblings in Utero Exposed to High Doses of 1,3-Butanediol during Organogenesis

1986 ◽  
Vol 5 (4) ◽  
pp. 189-196 ◽  
Author(s):  
R. F. Mankes ◽  
V. Renak ◽  
J. Fieseher ◽  
R. Lefevre
Keyword(s):  
Developmental Toxicity ◽  
In Utero ◽  
Cellular Damage ◽  
Male Rats ◽  
Body Weights ◽  
Fetal Repair ◽  
Dose Dependent Decrease ◽  
High Doses ◽  
Embryotoxic Effects ◽  
Dose Dependent

The embryotoxic effects of high doses of the narcotizing ethanol dimer 1,3-butanediol were evaluated in pregnant Long-Evans rats during the “critical period” of organogenesis. Butanediol was given by gavage at levels of 0,7060,4236, or 706 mg/kg per day (24,14.4, or 2.4% of the acute oral LD50 value for rats). Maternal sedation was observed at 7060 and 4236 mg/kg, but feed consumptions and maternal body weights were unaffected. Butanediol caused a significant, dose-dependent decrease in offspring birthweights. At the highest butanediol dose, birthweights were preferentially and significantly decreased in male pups not contiguous in utero to female siblings. Other group I1 offspring were not affected and did not differ significantly from controls. As butanediol was given prior to the period of greatest fetal growth and fetal sex steroidogenests, it is concluded that intra-uterine levels of female sex steroids (estradiol) enhance fetal repair of cellular damage (restitution ad integrum), whereas testosterone inhibits fetal repair or exacerbates previous embryonic damage by some unknown mechanism. Such interaction furthers the concept that intrauterine position affects the endpoints of developmental toxicity, as expressed at partuition.

ACUTE EFFECTS OF SYNTHETIC PORCINE CALCITONINS ON THE RENAL EXCRETION OF MAGNESIUM, INORGANIC PHOSPHATE, SODIUM AND POTASSIUM

1971 ◽  
Vol 51 (3) ◽  
pp. 455-464 ◽  
Author(s):  
S. PORS NIELSEN ◽  
B. BUCHANAN-LEE ◽  
E. W. MATTHEWS ◽  
J. M. MOSELEY ◽  
C. C. WILLIAMS
Keyword(s):  
Inorganic Phosphate ◽  
Renal Excretion ◽  
Performic Acid ◽  
Male Rats ◽  
Acid Oxidation ◽  
Acute Effects ◽  
Dose Dependent Decrease ◽  
Magnesium Excretion ◽  
Dose Dependent ◽  
Sodium And Potassium

SUMMARY Synthetic porcine calcitonin (α-calcitonin) and its methionine-sulphoxide derivative (β-calcitonin) were given by intravenous infusion to conscious male rats. α-Calcitonin inactivated by performic acid oxidation was used as a control. Microgram doses of α-calcitonin produced a dose-dependent decrease in the renal excretion of magnesium. The effect was not due to a secondary release of parathyroid hormone since it was also seen in parathyroidectomized animals. A marked increase in the renal excretion of inorganic phosphate, sodium and potassium preceded the change in magnesium excretion in parathyroidectomized rats. It is concluded that the phosphaturia and natriuresis previously described after administration of extracted calcitonin preparations are true effects of the hormone. The effect of β-calcitonin was indistinguishable from that of α-calcitonin.

THE EFFECTS OF TESTOSTERONE AND ITS 5α-REDUCED METABOLITES ON PITUITARY RESPONSIVENESS TO GONADOTROPHIN-RELEASING HORMONE (Gn-RH)

1977 ◽  
Vol 86 (4) ◽  
pp. 728-732 ◽  
Author(s):  
Y. Epstein ◽  
B. Lunenfeld ◽  
Z. Kraiem
Keyword(s):  
Pituitary Gland ◽  
Mature Male ◽  
Male Rats ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Low Levels ◽  
High Doses ◽  
Dose Dependent ◽  
Stimulation Of

ABSTRACT The aim of this study was to investigate effects of androgens on gonadotrophin release in response to gonadotrophin-releasing hormone (Gn-RH) stimulation in vitro. Hemipituitaries of mature male rats were pre-incubated for 90 min with T, DHT, 3α- or 3β-diol (4 ng or 4 μg/ml medium), and the incubation continued for 240 min after adding Gn-RH (1 ng/ml medium). Gn-RH caused a 4-5-fold rise in the secretion of LH and a 2-fold rise in FSH secretion. The effect of the androgens was dose-dependent. At low levels, T and DHT exerted no effect on Gn-RH-stimulated gonadotrophin release, whereas the two androstanediols (3α- and 3β-diol) augmented the Gn-RH stimulation of both gonadotrophins, though preferentially LH. With high doses of androgens, the results obtained showed: a) no effect of T; b) DHT suppression of the Gn-RH-stimulated FSH release; c) suppression of Gn-RH stimulation by 3α- and 3β-diol regarding both LH and FSH. It is concluded that T exerts through its reduced metabolites a feedback effect on the pituitary gland responsiveness to Gn-RH stimulation.

scholarly journals Stepwise Embryonic Toxicity of Silver Nanoparticles onOryzias latipes

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Jae-Gu Cho ◽  
Kyung-Tae Kim ◽  
Tae-Kwon Ryu ◽  
Jae-woo Lee ◽  
Ji-Eun Kim ◽  
...  
Keyword(s):  
Heart Rate ◽  
Silver Nanoparticles ◽  
Embryonic Development ◽  
Developmental Stages ◽  
Developmental Toxicity ◽  
Heart Beat ◽  
Hatching Rate ◽  
Dose Dependent Decrease ◽  
Embryonic Toxicity ◽  
Dose Dependent

The developmental toxicity of silver nanoparticles (AgNPs) was investigated following exposure ofOryzias latipes(medaka) embryos to 0.1−1 mg/L of homogeneously dispersed AgNPs for 14 days. During this period, developmental endpoints, including lethality, heart rate, and hatching rate, were evaluated by microscopy for different stages of medaka embryonic development. To compare toxic sensitivity, acute adult toxicity was assessed. There was no difference in acute lethal toxicity between embryo and adult medaka. Interestingly, we found that the increase in stepwise toxicity was dependent on the developmental stage of the embryo. Lethal embryonic toxicity increased from exposure days 1 to 3 and exposure days 5 to 8, whereas there was no change from exposure days 3 to 5. In addition, 7 d exposure to 0.8 mg/L AgNPs resulted in significant heart beat retardation in medaka embryos. AgNPs also caused a dose-dependent decrease in the hatching rate and body length of larvae. These results indicate that AgNP exposure causes severe developmental toxicity to medaka embryos and that toxicity levels are enhanced at certain developmental stages, which should be taken into consideration in assessments of metallic NPs toxicity to embryos.

Antioxidant Effect of Stevia Rebaudiana on Humanerythrocytes

2020 ◽  
Vol 2 (29) ◽  
pp. 26-31
Author(s):  
Mohd Abu Zaid Yamini Anand
Keyword(s):  
Free Radicals ◽  
Stevia Rebaudiana ◽  
The Body ◽  
Cellular Damage ◽  
Glutathione S Transferase ◽  
Toxic Heavy Metals ◽  
Synthetic Chemicals ◽  
Dose Dependent Decrease ◽  
Dose Dependent

Abstract-The changing lifestyle and environment conditions have predisposed common man towards numerous diseases. Today most of the diseases are said to be caused by synthetic chemicals, toxic heavy metals, and the stress of modern living. It is also true that oxygen is essential for sustaining life but it is also dangerous to our existence. Oxygen is being viewed as playing a lead role in the generation of reactive intermediates, thereby causing cellular damage. Our body has the mechanism to handle free radicals and prevent its damaging effect, which involves the use of antioxidants as glutathione and antioxidant enzymes assuperoxidedismutase,catalase,glutathioneperoxidaseglutathionereductase, glutathione-S-transferase to counter these free radicals. When the redoxstatus of the body is overwhelmed by these radical species, this may result in variety of chronic diseases and even premature senility.The administration of natural antioxidant as food constitutes or therapeutic agents is looked-for to neutralize these reactive oxygen species and prevent or delay diseased condition caused by these reactive species. Most exogenous antioxidants come from raw vegetable fruits, spices, herbsandvariousmedicinalplants.Naturalantioxidants are always appreciated over synthetic ones because they lack toxic side effects. The present study deals with the effectsofStevia rebaudiana leaf extract on the statusantioxidant of RBC as evident by an in vitro dose-dependent decrease in the activity of erythrocytes superoxide dismutaseand catalase as compared to the normal control whereas at much higher concentration ofstevialeaf extract (100μg/ml)started to show a reversingtrendofitsprotectiveaction.

NON-SELECTIVE INHIBITION OF BASAL GLUCAGON RELEASE BY [d-CYS14]-ANALOGUES OF SOMATOSTATIN IN THE RAT

1979 ◽  
Vol 81 (3) ◽  
pp. 315-323 ◽  
Author(s):  
FRITZ MÄRKI ◽  
BRUNO KAMBER ◽  
HANS RINK ◽  
PETER SIEBER
Keyword(s):  
Time Course ◽  
Dose Range ◽  
Subcutaneous Administration ◽  
Selective Inhibition ◽  
Glucagon Release ◽  
Basal Plasma ◽  
Dose Dependent Decrease ◽  
High Doses ◽  
Glucagon And Insulin ◽  
Dose Dependent

The effects of two [d-Cys14]-analogues of somatostatin on basal plasma levels of glucagon, insulin and glucose were determined in unanaesthetized rats to re-examine a glucagon-selective action of these peptides which has been claimed by others. Somatostatin, [d-Cys14]-somatostatin and [d-Trp8, d-Cys14]-somatostatin caused a short-lasting, dose-dependent decrease of plasma glucagon and insulin but they had no significant influence on plasma glucose. Glucagon and insulin reached the nadir 2 min after intravenous injection of the peptides (dose range 1–10 μg/kg) or 5 min after subcutaneous administration (30 and 300 μg/kg). At the nadir, insulin was decreased to a greater extent than glucagon and the effects of all three peptides were equipotent. However, in the period after the nadir and at high doses, the time-course of some effects of the analogues on either glucagon or insulin differed from that of somatostatin. Thus, these [d-Cys14]-analogues may show partial kinetic dissociation of effects on glucagon and insulin but they are not truly selective inhibitors of glucagon release.

Selective pulmonary vasodilation with ATP-MgCl2 during pulmonary hypertension in lambs

1990 ◽  
Vol 69 (5) ◽  
pp. 1836-1842 ◽  
Author(s):  
J. R. Fineman ◽  
M. R. Crowley ◽  
S. J. Soifer
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Systemic Arterial Pressure ◽  
Pulmonary Vasodilation ◽  
Potent Vasodilator ◽  
Pulmonary Arterial ◽  
Dose Dependent Decrease ◽  
High Doses ◽  
Dose Dependent

We investigated the effects of infusions of ATP-MgCl2 on the circulation in 11 spontaneously breathing newborn lambs during pulmonary hypertension induced either by the infusion of U-46619, a thromboxane A2 mimetic, or by hypoxia. During pulmonary hypertension induced by U-46619, ATP-MgCl2 (0.01-1.0 mg.kg-1.min-1) caused a significant dose-dependent decrease in pulmonary arterial pressure (12.4-40.7%, P less than 0.05), while systemic arterial pressure decreased only at the highest doses (P less than 0.05). Left atrial infusions of ATP-MgCl2 caused systemic hypotension without decreasing pulmonary arterial pressure. During hypoxia-induced pulmonary hypertension, ATP-MgCl2 caused a similar significant dose-dependent decrease in pulmonary arterial pressure (12.0-41.1%, P less than 0.05), while systemic arterial pressure decreased only at high doses (P less than 0.05). Regression analysis showed selectivity of the vasodilating effects of ATP-MgCl2 for the pulmonary circulation during pulmonary hypertension induced either by U-46619 or hypoxia. ATP-MgCl2 is a potent vasodilator with a rapid metabolism that allows for selective vasodilation of the vascular bed first encountered (pulmonary or systemic). We conclude that infusions of ATP-MgCl2 may be clinically useful in the treatment of children with pulmonary hypertension.

scholarly journals Inhibition of rat brain and human red cell acetylcholinesterase by thiocarbamate herbicides

2020 ◽  
Vol 9 (5) ◽  
pp. 591-600
Author(s):  
Edward A Lock
Keyword(s):  
Rat Brain ◽  
Male Rats ◽  
Red Cell ◽  
Toxicological Evaluation ◽  
Agricultural Industry ◽  
Cell Enzyme ◽  
Reproductive Impairment ◽  
High Doses ◽  
Dose Dependent

Abstract Thiocarbamates are a major class of herbicides that were used extensively in the agricultural industry. Toxicological evaluation showed molinate caused reproductive impairment in male rats, whilst others produced behavioural effects at high doses. Rats dosed with molinate either as a single large oral dose of 100 mg/kg or as multiple doses of 50 mg/kg for 7 days produced inhibition of brain acetylcholinesterase (AChE). Molinate and other thiocarbamate herbicides undergo metabolism to form sulphoxides that can carbamoylate thiol’s such as glutathione and proteins. We have chemically synthesised the sulphoxide and sulphone metabolites of six thiocarbamate herbicides and examined their ability to inhibit rat brain and human red cell AChE in vitro. Parent thiocarbamates were inactive, whilst the sulphoxides produced inhibition with IC50’s in the 1–10 mM range, the sulphone metabolites were the most active with IC50’s for molinate, pebulate, EPTC and vernolate in the μM range. Inhibition was both time- and dose-dependent with biomolecular rate constants for the inhibition of the human red cell enzyme of 0.3 × 102 and 2.0 × 102 M−1 min−1 for molinate sulphoxide and sulphone, respectively. No recovery of enzyme activity, with either enzyme, was seen following dilution of the inhibitor to a concentration that does not inhibit the enzyme for up to 24 h at 25°C at pH 7.4. The metabolites of these thiocarbamate herbicides are rather poor inhibitors of AChE when compared to the organophosphorus ester, paraoxon or the monomethylcarbamate, eserine. Unlike eserine the inhibition produced by the thiocarbamates is irreversible.

Ultrastructural Localization of Acetylcholinesterase in the Arcuate Nucleus and Median Eminence of the Rat

1977 ◽  
Vol 35 ◽  
pp. 440-441
Author(s):  
K.A. Carson ◽  
C.B. Nemeroff ◽  
M.S. Rone ◽  
J.S. Kizer ◽  
J.S. Hanker
Keyword(s):  
Choline Acetyltransferase ◽  
Median Eminence ◽  
Arcuate Nucleus ◽  
Cholinergic Neurons ◽  
Ultrastructural Localization ◽  
Male Rats ◽  
Neonatal Rats ◽  
Good Marker ◽  
Chemical Studies ◽  
High Doses

Biochemical, physiological, pharmacological, and more recently enzyme histo- chemical data have indicated that cholinergic circuits exist in the hypothalamus. Ultrastructural correlates of these pathways such as acetylcholinesterase (AchE) positive neurons in the arcuate nucleus (ARC) and stained terminals in the median eminence (ME) have yet to be described. Initial studies in our laboratories utilizing chemical lesioning and microdissection techniques coupled with microchemical and light microscopic enzyme histo- chemical studies suggested the existence of cholinergic neurons in the ARC which project to the ME (1). Furthermore, in adult male rats with Halasz deafferentations (hypothalamic islands composed primarily of the isolated ARC and the ME) choline acetyltransferase (ChAc) activity, a good marker for cholinergic neurons, was not significantly reduced in the ME and was only somewhat reduced in the ARC (2). Treatment of neonatal rats with high doses of monosodium 1-glutamate (MSG) results in a lesion largely restricted to the neurons of the ARC.

Melatonin actions in the heart; more than a hormone

2018 ◽  
Vol 1 (1) ◽  
pp. 21-26 ◽  
Author(s):  
Darío Acuña-Castroviejo ◽  
Maria T Noguiera-Navarro ◽  
Russel J Reiter ◽  
Germaine Escames
Keyword(s):  
Cell Membranes ◽  
Myocardial Cell ◽  
Rat Tissues ◽  
Dependent Manner ◽  
Broad Distribution ◽  
Multiple Organs ◽  
High Doses ◽  
Extrapineal Melatonin ◽  
Dose Dependent ◽  
Different Doses

Due to the broad distribution of extrapineal melatonin in multiple organs and tissues, we analyzed the presence and subcellular distribution of the indoleamine in the heart of rats. Groups of sham-operated and pinealectomized rats were sacrificed at different times along the day, and the melatonin content in myocardial cell membranes, cytosol, nuclei and mitochondria, were measured. Other groups of control animals were treated with different doses of melatonin to monitor its intracellular distribution. The results show that melatonin levels in the cell membrane, cytosol, nucleus, and mitochondria vary along the day, without showing a circadian rhythm. Pinealectomized animals trend to show higher values than sham-operated rats. Exogenous administration of melatonin yields its accumulation in a dose-dependent manner in all subcellular compartments analyzed, with maximal concentrations found in cell membranes at doses of 200 mg/kg bw melatonin. Interestingly, at dose of 40 mg/kg b.w, maximal concentration of melatonin was reached in the nucleus and mitochondrion. The results confirm previous data in other rat tissues including liver and brain, and support that melatonin is not uniformly distributed in the cell, whereas high doses of melatonin may be required for therapeutic purposes.

Sign in / Sign up

Export Citation Format

Share Document