THE MECHANISM OF THE PROTECTIVE ACTION OF CLAMPING THE RENAL PEDICLES OF DOGS WITH ALLOXAN DIABETES

Clamping of the renal vessels gives rise to a reflex change of circulation at the level of the vascular zone innervated by the splanchnic nerves. Bilateral cutting of the splanchnic nerves and of the inferior part of the sympathetic chain at the level of the thorax prevents the reflex, and annuls the protective action of clamping the vascular pedicles of the kidney. Renal lesions are not absolutely necessary for the production of alloxan diabetes, but may aggravate diabetes, probably by adding the toxic effects of retention of urine.

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Protective Role of Flavonoids against Intestinal Pro-Inflammatory Effects of Silver Nanoparticles

Molecules ◽

10.3390/molecules26216610 ◽

2021 ◽

Vol 26 (21) ◽

pp. 6610

Author(s):

Ana T. Rufino ◽

Ana Ramalho ◽

Adelaide Sousa ◽

José Miguel P. Ferreira de Oliveira ◽

Paulo Freitas ◽

...

Keyword(s):

Silver Nanoparticles ◽

Protective Action ◽

Cell Types ◽

Protective Role ◽

Toxic Effects ◽

Oral Exposure ◽

Dietary Flavonoids ◽

Harmful Effects ◽

Human Intestinal Cells

Silver nanoparticles (AgNP) have been increasingly incorporated into food-related and hygiene products for their unique antimicrobial and preservative properties. The consequent oral exposure may then result in unpredicted harmful effects in the gastrointestinal tract (GIT), which should be considered in the risk assessment and risk management of these materials. In the present study, the toxic effects of polyethyleneimine (PEI)-coated AgNP (4 and 19 nm) were evaluated in GIT-relevant cells (Caco-2 cell line as a model of human intestinal cells, and neutrophils as a model of the intestinal inflammatory response). This study also evaluated the putative protective action of dietary flavonoids against such harmful effects. The obtained results showed that AgNP of 4 and 19 nm effectively induced Caco-2 cell death by apoptosis with concomitant production of nitric oxide, irrespective of the size. It was also observed that AgNP induced human neutrophil oxidative burst. Interestingly, some flavonoids, namely quercetin and quercetagetin, prevented the deleterious effects of AgNP in both cell types. Overall, the data of the present study provide a first insight into the promising protective role of flavonoids against the potentially toxic effects of AgNP at the intestinal level.

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Toxic effects caused by heavy metals in the yeast Saccharomyces cerevisiae: a comparative study

Canadian Journal of Microbiology ◽

10.1139/w03-044 ◽

2003 ◽

Vol 49 (5) ◽

pp. 336-343 ◽

Cited By ~ 45

Author(s):

Eduardo V Soares ◽

Kristel Hebbelinck ◽

Helena MVM Soares

Keyword(s):

Heavy Metals ◽

Saccharomyces Cerevisiae ◽

Protective Action ◽

Toxic Effects ◽

Nickel Metal ◽

Yeast Saccharomyces Cerevisiae ◽

Copper Complexation ◽

Ph Buffer ◽

Ethanesulfonic Acid ◽

Copper Lead

The decreasing order of toxicity of select heavy metals on the yeast Saccharomyces cerevisiae, in 10 mM MES (2-(N-morpholino)ethanesulfonic acid) pH buffer at pH 6.0, was found to be copper, lead, and nickel. Heavy metal (200 µM) induced a decrease in the number of viable cells by about 50% in the first 5 min for copper and in 4 h for lead, while nickel was not toxic up to a 200 µM concentration over a period of 48 h. Glucose (25 mM) strongly enhanced the toxic effect of 50 µM copper but had little or no effect on the toxicity of 200 µM lead or nickel. Copper, lead, and nickel induced the leakage of UV260-absorbing compounds from cells with different kinetics. The addition of 0.5 mM calcium, before addition of 200 µM copper, showed a protective action against cell death and decreased the release of UV-absorbing compounds, while no effect was observed against lead or nickel toxic effects. Copper complexation capacities of the filtrates of cells exposed for 2 h in 200 µM copper and 24 h in 200 µM lead were 51 and 14 µM, respectively. The implication of the complexation shown by these soluble compounds in the bioavailability of heavy metals is discussed.Key words: copper, lead, nickel, metal bioavailability, toxicity.

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RENAL LESIONS IN RATS WITH LONG-TERM ALLOXAN DIABETES

Acta Pathologica Microbiologica Scandinavica Section A Pathology ◽

10.1111/j.1699-0463.1974.tb03844.x ◽

2009 ◽

Vol 82A (2) ◽

pp. 199-210

Author(s):

Erik Hägg

Keyword(s):

Alloxan Diabetes ◽

Renal Lesions

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Endotoxin-tolerant rats are still protected from oxygen toxicity by low-dose endotoxin treatment

Journal of Applied Physiology ◽

10.1152/jappl.1985.58.3.819 ◽

1985 ◽

Vol 58 (3) ◽

pp. 819-822 ◽

Cited By ~ 7

Author(s):

L. Frank

Keyword(s):

Low Dose ◽

Protective Action ◽

Lethal Dose ◽

Oxygen Toxicity ◽

Exposure Period ◽

Lung Damage ◽

Toxic Effects ◽

Beneficial Effects ◽

High Degree ◽

Tolerant State

To determine if we could reduce endotoxin's potential for toxicity, we produced “endotoxin-tolerant” rats by administering progressively increasing daily doses of endotoxin (10 ng, 100 ng, 1 microgram, 10 micrograms/kg). This dosage regimen produced a high degree of tolerance to the toxic actions of endotoxin: whereas only 3/17 (18%) of control rats survived a normally lethal dose of endotoxin (25 mg/kg), survival for the endotoxin-tolerant rats was 16/16. When endotoxin-tolerant rats received a standard protective dose of 500 micrograms/kg endotoxin just before transfer to 96–98% O2, 19/20 survived the 72-h exposure period vs. 20–30% survival for controls. Thus whereas the endotoxin-tolerant state blocked the tested lethal and toxic effects of endotoxin, it did not nullify the O2 protective action of endotoxin. In addition, endotoxin's stimulatory effects on the lung antioxidant enzymes in the 96–98% O2-exposed rats was also not blocked by the endotoxin-tolerant state. Thus the therapeutic ratio (TR) of endotoxin as an experimental pharmacological treatment against O2-induced lung damage has been markedly enhanced (TR = ratio of dose producing beneficial effects to dose producing toxic effects).

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On the anatomical organization of the lumbosacral sympathetic chain and the lumbar splanchnic nerves of the cat—Langley revisited

Journal of the Autonomic Nervous System ◽

10.1016/0165-1838(85)90044-x ◽

1985 ◽

Vol 12 (4) ◽

pp. 289-300 ◽

Cited By ~ 25

Author(s):

R. Baron ◽

W. Jänig ◽

Elspeth M. McLachlan

Keyword(s):

Sympathetic Chain ◽

Splanchnic Nerves

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Ultrastructure of the effect of T-514 obtained from Karwinskia humboldtiana on assembly and integrity of yeast's peroxisomes

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100084983 ◽

1991 ◽

Vol 49 ◽

pp. 136-137

Author(s):

J. Sepulveda-Saavedra ◽

I. Vander-Klei ◽

M. Venhuis ◽

Y. Piñeyro-Lopez

Keyword(s):

Culture Conditions ◽

Toxic Effects ◽

Candida Boidinii ◽

Central Mexico ◽

Poisonous Plant ◽

Biological Behaviour ◽

Enzyme Content ◽

Fat Deposits ◽

Yeast Model

Karwinskia humboldtiana is a poisonous plant that grows in semi desertic areas in north and central México. It produces several substances with different toxic effects. One of them designated T-514 damages severely the lung, kidney and liver, producing in the hepatoeyte large intracellular fat deposits and necrosis. Preliminary observations demonstrated that three is a decrease in the amount of peroxisomes in the hepatocytes of experimentally intoxicated rats and monkeys. To study the effect exerted by the T-514 on peroxisomes, a yeast model was selected, thus, three species: Saccha romices cerevisiae, Ilansenula polymorpha and Candida boidinii were used, because there is information concerning their peroxisome's morphology, enzyme content, biological behaviour under different culture conditions and biogenesis.

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Some Conditions Necessary for Pinocytosis

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100100457 ◽

1968 ◽

Vol 26 ◽

pp. 142-143

Author(s):

M. W. Brightman

Keyword(s):

Smooth Muscle ◽

Cell Membrane ◽

Toxic Effects ◽

Cytological Evidence ◽

Cell Processes

The cytological evidence for pinocytosis is the focal infolding of the cell membrane to form surface pits that eventually pinch off and move into the cytoplasm. This activity, which can be inhibited by oxidative and glycolytic poisons, is performed only by cell processes that are at least 300A wide. However, the interpretation of such toxic effects becomes equivocal if the membrane invaginations do not normally lead to the formation of migratory vesicles, as in some endothelia and in smooth muscle. The present study is an attempt to set forth some conditions under which pinocytosis, as distinct from the mere inclusion of material in surface invaginations, can take place.

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