Low concentrations of sodium arsenite induce hepatotoxicity in prepubertal male rats

2020 ◽  
Vol 35 (5) ◽  
pp. 553-560 ◽  
Author(s):  
Ricardo R. Samelo ◽  
Paloma Cunha de Medeiros ◽  
Deborah N. Carvalho Cavalcante ◽  
Maria L. G. Aranha ◽  
Fabio A. Duarte ◽  
...  
Keyword(s):  
Sodium Arsenite ◽  
Male Rats ◽  
Low Concentrations

scholarly journals Structures of the somatotropin receptor and prolactin receptor on rat hepatocytes characterized by affinity labelling

1984 ◽  
Vol 220 (2) ◽  
pp. 361-369 ◽  
Author(s):  
K Yamada ◽  
D B Donner
Keyword(s):  
Binding Sites ◽  
Prolactin Receptor ◽  
Rat Hepatocytes ◽  
Membrane Receptors ◽  
Bovine Somatotropin ◽  
Male Rats ◽  
Disulphide Bonds ◽  
Low Concentrations ◽  
Affinity Labelling ◽  
Structural Descriptions

Human somatotropin competed for 125I-human somatotropin binding to hepatocytes from female or male rats. Bovine somatotropin and prolactin each inhibited part, but not all, of the uptake of 125I-human somatotropin. The binding of 125I-prolactin was inhibited by human somatotropin and prolactin, but not by bovine somatotropin. Bovine somatotropin and human somatotropin, but not prolactin, competed for 125I-bovine somatotropin binding sites. 125I-labelled hormones were covalently coupled to membrane receptors with higher efficiency on hepatocytes from female than from male rats, allowing structural descriptions of lactogenic and somatogenic binding sites that had not been possible previously. Disuccinimidyl suberate covalently coupled 125I-human somatotropin into saturable complexes of Mr 300 000, 220 000, 130 000, 65 000 and 50 000. Bovine somatotropin inhibited the incorporation of 125I-human somatotropin into complexes of Mr 300 000, 220 000 and 130 000, whereas low concentrations of prolactin competed for incorporation into the 65 000- and 50 000-Mr species. 125I-bovine somatotropin was incorporated into complexes of Mr 300 000, 220 000 and 130 000. Human somatotropin and bovine somatotropin, but not prolactin, inhibited the production of these complexes. 125I-prolactin binding produced complexes of Mr 65 000 and 50 000. Native prolactin and human somatotropin, but not bovine somatotropin, inhibited uptake of 125I-prolactin into these species. Thus direct affinity labelling, as well as competition for covalent coupling, suggests that the 300 000-, 220 000- and 130 000-Mr species are components of the somatotropin receptor and that the 65 000- and 50 000-Mr complexes result from hormone binding to the prolactin receptor. By subtracting the Mr of prolactin, it was calculated that the hormone was bound to species of Mr 43 000 and 28 000. These Mr values were not affected by reduction of solubilized membranes, suggesting that the structure of the prolactin receptor is not stabilized by interchain disulphide bonds between subunits. Subtracting the Mr of somatotropin from somatogenic complexes indicated that the hormone had bound to species of Mr 280 000, 200 000 and 100 000. The 300 000- and 220 000-Mr complexes were not isolated from reduced membranes, whereas the amount of the 130 000-Mr species was augmented. These observations could suggest that a major component of the somatotropin receptor is a trimeric aggregate in which some subunits are retained in a larger complex by interchain disulphide bonds.

scholarly journals Influence of elevated content of cadmium and arsenic in diet containing feeding yeast on organisms of rats

2009 ◽  
Vol 54 (No. 1) ◽  
pp. 1-9 ◽  
Author(s):  
J. Száková ◽  
V. Zídek ◽  
D. Miholová
Keyword(s):  
Sodium Arsenite ◽  
Cadmium Accumulation ◽  
Yeast Cells ◽  
Male Rats ◽  
Arsenic Content ◽  
Cadmium Content ◽  
Cd Accumulation ◽  
Experimental Animals ◽  
Natural Level ◽  
Liver And Kidney

The influence of elevated cadmium content in diet on the content of this element in liver, kidney and testes of 68 male rats was studied in dependence on the chemical form of applied cadmium (as inorganic salt – CdCl<sub>2</sub> and organically bound in yeast cells); the influence of elevated arsenic content (as NaAsO<sub>2</sub>) in diet on its content in the same organs was also investigated. The interactions between arsenic and cadmium in the above-mentioned organs were studied. The addition of cadmium to the diet of rats significantly (<I>P</I> < 0.05) increased cadmium content in several organs. The addition of yeast containing the natural level of Cd increased the content of cadmium in liver and kidney of experimental animals significantly (<I>P</I> < 0.05). A significantly (<I>P</I> < 0.05) increased cadmium accumulation in organs was observed after the addition of Cd as CdCl<sub>2</sub>, compared with the addition of Cd as organically bound Cd in yeast cells. At the same time, the addition of yeasts containing the natural level of Cd decreased the Cd accumulation applied as CdCl2 in the examined organs. The addition of sodium arsenite to the diet of rats led to a significantly (<I>P</I> < 0.05) increased arsenic content in all the analyzed organs. The addition of yeasts to the diet increased arsenic content in liver and at the same time suppressed its content in kidneys of experimental animals. The interaction between arsenic and cadmium applied simultaneously was evident. The addition of As to the diet decreased the accumulation of Cd in kidney and increased its accumulation in testes. The addition of Cd to the diet increased arsenic content in liver and kidney and decreased its content in testes.

Thapsigargin stimulates increased NO activity in hypoxic hypertensive rat lungs and pulmonary arteries

1996 ◽  
Vol 80 (4) ◽  
pp. 1336-1344 ◽  
Author(s):  
M. Muramatsu ◽  
R. C. Tyler ◽  
D. M. Rodman ◽  
I. F. McMurtry
Keyword(s):  
Pulmonary Artery ◽  
Chronic Hypoxia ◽  
Pulmonary Arteries ◽  
Male Rats ◽  
Pulmonary Vasculature ◽  
No Production ◽  
Low Concentrations ◽  
Pulmonary Vascular Endothelium ◽  
Increased Sensitivity ◽  
Stimulation Of

This study addressed the controversy of whether endothelium-derived nitric oxide (NO) activity is increased or decreased in the hypertensive pulmonary vasculature of chronically hypoxic rats. Thapsigargin, a receptor-independent Ca2+ agonist and stimulator of endothelial NO production, was used to compare NO-mediated vasodilation in perfused lungs and conduit pulmonary artery rings isolated from adult male rats either kept at Denver's altitude of 5,280 ft (control pulmonary normotensive rats) or exposed for 4-5 wk to the simulated altitude of 17,000 ft (chronically hypoxic pulmonary hypertensive rats). Under baseline conditions, thapsigargin (10(-9)-10(-7) M) caused vasodilation in hypertensive lungs and vasoconstriction in normotensive lungs. Whereas the sustained vasodilation in hypertensive lungs was reversed to vasoconstriction by the inhibitor of NO synthase N(omega)-nitro-L-arginine (L-NNA; 10(-4) M), a transient vasodilation to thapsigargin in acutely vasoconstricted normotensive lungs was potentiated. As measured by a chemiluminescence assay, the recirculated perfusate of hypertensive lungs accumulated considerably higher levels of NO-containing compounds that did normotensive lungs, and thapsigargin-induced stimulation of NO-containing compounds accumulation was greater in hypertensive than in normotensive lungs. Similarly, low concentrations of thapsigargin (10(-10)-10(-9) M) caused greater endothelium-dependent L-NNA-reversible relaxation of hypertensive than of normotensive pulmonary artery rings. The increased sensitivity of hypertensive arteries to thapsigargin-induced relaxation was eliminated in nominally Ca(2+)-free medium and was not mimicked by ryanodine, a releaser of intracellular Ca2+. These results with thapsigargin, which acts on endothelial cells to stimulate Ca2+ influx and a sustained rise in intracellular Ca2+ concentration, support the idea that pulmonary vascular endothelium-derived NO activity is increased rather than decreased in chronic hypoxia-induced pulmonary hypertension in rats.

Potentiation of toxicity of Sumithion by phosphamidon in the rat

1968 ◽  
Vol 46 (2) ◽  
pp. 133-137 ◽  
Author(s):  
P. E. Braid ◽  
M. Nix
Keyword(s):  
Female Rats ◽  
Male Rats ◽  
Conversion Reaction ◽  
Oral Dosing ◽  
Low Concentrations ◽  
Potentiation Of Toxicity

Acute oral dosing of male rats with mixtures of Sumithion and phosphamidon produces a marked potentiation of toxicity as evidenced by increased mortality. While potentiation also occurs with female rats dosed with mixtures containing relatively low concentrations of Sumithion, the effect diminishes as the Sumithion concentration is increased. It is concluded that this potentiation is associated with a nonlinear thiophosphate conversion reaction.

scholarly journals Cytokine regulation of inflammatory processes in respiratory organs of rats exposed to the combined inhalation of chemicals in low concentrations

2021 ◽  
Vol 100 (3) ◽  
pp. 290-294
Author(s):  
Maria Yu. Barantseva ◽  
Lana N. Mukhamedieva ◽  
Olga A. Dadasheva ◽  
Dmitry S. Ozerov ◽  
Anna A. Pakhomova ◽  
...  
Keyword(s):  
Lung Tissue ◽  
Structural Changes ◽  
Transforming Growth Factor ◽  
Recovery Period ◽  
Male Rats ◽  
Interleukin 4 ◽  
Tracheal Wall ◽  
Enzyme Linked Immunosorbent Assay ◽  
Morphological Studies ◽  
Low Concentrations

Introduction. Morphological studies of animals (trachea, bronchi, lungs) exposed to the combined inhalation of chemicals in low concentrations showed the progression of structural changes, indicating the activation of inflammation and fibrosis in the lungs. The role of cytokine markers in developing inflammatory and fibrotic processes and remodeling lung tissue has been studied. Materials and methods. Male rats (180-200 g) were exposed to a mixture of chemicals (acetone, acetaldehyde, benzene) in low concentrations of 0.7-1.5; 0.9-1.4; 0.2-0.4 (mg/m3), respectively. The concentrations of IL-6, IL-10, IL-1b, IL-4, TGFβ1, TNFα cytokines (pg/ml) have been measured in the lung homogenate by enzyme-linked immunosorbent assay (ELISA). Microscopic anatomy of the lungs, tracheal wall, bronchi has been studied on the 30th day of exposure and the 15th and 90th days of the recovery period. Results. An increase in interleukin-4 and transforming growth factor TGFβ1 in the homogenate of the lung tissue was shown. An increase in lymphatic follicles, the number of lymphocytes, neutrophils, macrophages, and focal accumulations of eosinophils has been observed in the tracheal wall. In lymphoid infiltrates of the lung tissue - eosinophils, macrophages, and plasmocytes. Accumulation of eosinophilic exudate has been observed in some alveoli. The 90th day of the recovery period is characterized by a significant increase of TGFβ1 in the lung tissue, indicating fibrosis, as evidenced by the rise in the number of fibroblasts between the alveoli in the atelectasis zones of lungs. Conclusion. The chronic combined exposure to the mixture of chemicals in low concentrations is accompanied by a pro-inflammatory process in the lungs with the type II hypersensitivity and increasing IL-4 and TGFβ1 (a key mediator of profibrotic activity).

scholarly journals Histopathological alterations in testicular tissue of male rats exposed to arsenic

2012 ◽  
Vol 4 (2) ◽  
pp. 247-251
Author(s):  
Reema Pachnanda ◽  
Shiv Pal Singh
Keyword(s):  
Body Weight ◽  
Sodium Arsenite ◽  
Testicular Tissue ◽  
The Body ◽  
Female Rats ◽  
Male Rats ◽  
Histological Evaluation ◽  
Seminiferous Tubules ◽  
Experimental Animals ◽  
Testicular Weight

The present study was designed to investigate the adverse effect of arsenic on testicular tissue of Swiss albino male rats. Sodium arsenite was administered to adult male rats by gavage at the doses 1, 2 and 3 mg/kg body weight for 30 days. After the treatment, the testis were processed for histopathological observations. Sodium arsenite caused remarkable reduction in testicular weight (P<0.05), while the body weight of experimental animals were reduced but not significantly (P<0.05). Histological evaluation revealed dose-dependent, gradual destruction in histoarchitecture of testicular tissue. Sodium arsenite exposure caused complete arrest of spermatogenesis with disfigured seminiferous tubules in the testes .The lumens of the tubules were devoid of spermatids and were in places filled with cellular debris. The germinal epithelium was distorted. At places interstitial odema was also evident. Sertoli and Leydig cells were damaged. Along with structural alterations, fertility rate in experimental animals was significantly decreased at higher doses i.e. 2 and 3 mg/kg, as 100% infertility was observed. After withdrawal of the treatment over a period of 30 days, recovery was observed in low dose groups as few female rats became pregnant. The study concluded that exposure of arsenic causes testicular toxicity in male albino rat.

scholarly journals Extraction, isolation and evaluation of anti-toxic principles from Moringa oleifera (MOF6) and Myristica fragrans (Trimyristin) upregulated Acetylcholinesterase concentrations in Sodium arsenite-induced neurotoxicity in rats.

2021 ◽  
Vol 19 (2) ◽  
pp. 466-482
Author(s):  
Adelaja Akinlolu ◽  
Mubarak Ameen ◽  
Tobilola Quadri ◽  
Kayode Odubela ◽  
Gabriel Omotoso ◽  
...  
Keyword(s):  
Moringa Oleifera ◽  
Sodium Arsenite ◽  
Statistical Significance ◽  
Physiological Saline ◽  
Male Rats ◽  
Neuroprotective Effects ◽  
Myristica Fragrans ◽  
Moringa Oleifera Leaves ◽  
Group 2 ◽  
Biochemical Analyses

This study evaluated the neuroprotective effects of MOF6 (isolated from Moringa oleifera leaves) and Trimyristin (isolated from Myristica fragrans seeds) on Acetylcholinesterase concentrations in cerebral cortices of rats with Sodium arsenite-induced neurotoxicity. Sixty-five adult male rats (150 g-250 g) were randomly divided into thirteen groups comprising of five rats per group. Groups 1 and 3 received physiological saline and 1 ml/200 g bodyweight of Olive oil respectively for 9 weeks. Group 2 received 20 mg/kg bodyweight of Sodium arsenite (SA) for 6 weeks and left untreated for another 3 weeks. Groups 4-5 received 20 mg/kg bodyweight of SA for 3 weeks followed by treatments with 5.0 and 7.5 mg/kg bodyweight of MOF6 respectively for 6 weeks. Groups 6-7 received 20 mg/kg bodyweight of SA for 3 weeks followed by treatments with 15 and 30 mg/kg bodyweight of Trimyristin respectively for 6 weeks. Groups 8-11 received 5.0 and 7.5 mg/kg bodyweight of MOF6; 15 and 30 mg/kg bodyweight of Trimyristin respectively for 9 weeks. Groups 12-13 received 7.5 mg/kg bodyweight of MOF6 and 30 mg/kg bodyweight of Trimyristin respectively for 6 weeks followed by co-administration of each extract dose with 20 mg/kg bodyweight of SA for another 3 weeks. Histological examination of cerebral cortices and biochemical analyses of Acetylcholinesterase concentrations were carried out in all rats. Computed data were analyzed using Microsoft Excel 2016 with statistical significance at p≤0.05. Histo-pathological evaluations revealed normal histo-architecture of cerebral cortices of all rats. Results showed statistically significant (p≤0.05) increases in Acetylcholinesterase concentrations in rats of Groups 1-10 and 12 compared with Group 2 (2.78±1.76 𝜇mole/min/g). 7.5 mg/kg bodyweight of MOF6 showed the best therapeutic and neuro-regenerative potential against SA-induced neurotoxicity.Conclusions: Our findings implied that MOF6 and Trimyristin reversed downregulation of Acetylcholinesterase concentrations in SA-induced neurotoxicity in rats; and possess neuro-protective and neuro-regenerative potentials.

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