Tumor necrosis factor-induced apoptosis during the poisoning of mice with hepatotoxins

Leist, Marcel; Gantner, Florian; Naumann, Heike; Bluethmann, Horst; Vogt, Kathrin; Brigelius‐Flohé, Regina; Nicotera, Pierluigi; Volk, Hans‐Dieter; Wendel, Albrecht

doi:10.1053/gast.1997.v112.pm9041255

Cited by 194 publications

(133 citation statements)

References 61 publications

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“…It is well characterized that NRF2 stimulates the antioxidant defense system in response to oxidative stress, and it could be speculated that the decreased expression of NRF2 by α-AMA may be involved in the cytotoxicity of α-AMA (36). Furthermore, tumor necrosis factoralpha aggravates the α-AMA cytotoxicity by a mechanism that may involve reactive oxygen species (37,38).…”

Section: Discussionmentioning

confidence: 99%

Evaluation and comparison of alpha- and beta-amanitin toxicity on MCF-7 cell line

Kaya¹,

Bayram²,

Yaykaşlı³

et al. 2014

Turk J Med Sci

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Section: Discussionmentioning

confidence: 99%

Evaluation and comparison of alpha- and beta-amanitin toxicity on MCF-7 cell line

Kaya¹,

Bayram²,

Yaykaşlı³

et al. 2014

Turk J Med Sci

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“…Notably, in several pathological conditions (e.g. brain ischemia; Linnik et al, 1995;Beilharz et al, 1995;Portera-Cailliau et al, 1995;Charriaut-Marlangue et al, 1996), liver damage by cytokines or toxins (Leist et al, 1995(Leist et al, , 1997b) demise can occur simultaneously by necrosis or apoptosis. Work in our laboratory and in collaboration with Dr SA Lipton and Dr S Orrenius has previously shown that the intensity of the same initial insult decides the prevalence of either apoptosis or necrosis (Dypbukt et al, 1994;Bonfoco et al, 1995).…”

Section: Energy Supply and Cell Death P Nicotera And M Leistmentioning

confidence: 99%

Energy supply and the shape of death in neurons and lymphoid cells

1997

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Apoptosis and necrosis are considered as conceptually distinct forms of cell death. Nevertheless, there is increasing evidence that classical apoptosis and necrosis represent only the extreme ends of a wide range of possible morphological and biochemical deaths. The two classical types of demise can occur simultaneously in tissues or cell cultures exposed to the same stimulus, and often the intensity of the same initial insult decides the prevalence of either apoptosis or necrosis. This suggests that, while some early events may be common to both types of cell death, a downstream controller may be required to direct cells towards the organised execution of apoptosis. We have recently shown that intracellular energy levels and mitochondrial function are rapidly compromised in necrosis, but not in apoptosis of neuronal cells. Then, we went on to show that pre-emptying human T cells of ATP switches the type of demise caused by two classic apoptotic triggers (staurosporin and CD95 stimulation) from apoptosis to necrosis. Conditions of controlled intracellular ATP depletion, which was obtained by blocking mitochondrial and/or glycolytic ATP generation, were used in combination with repletion of the cytosolic ATP pool with glucose to redirect the death program towards apoptosis or necrosis. At least two distinct steps, the typical nuclear degradation, and the expression of annexin V-recognisable determinants on the cell surface require sufficient ATP generation. This suggests that some upstream regulators of cell death may be common to both types of cell demise, whereas yet unknown downstream processes decide its shape and the implications for the neighbouring tissue.

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“…In actinomycin D-primed C3H/HeJ mice treated intraperitoneally with SEB, liver injury was initially characterized by mild congestion, accumulation of polymorphonuclear leukocytes in sinusoids, and later by focal necrosis of hepatocytes (9). Actinomycin D itself also caused apoptosis of hepatocytes (19). Our intranasal SEB-induced murine toxic shock model showed that SEB itself could provoke liver congestion, apoptosis of hepatocytes, and portal inflammation.…”

Section: Morbidity and Mortalitymentioning

confidence: 72%

Murine Lethal Toxic Shock Caused by Intranasal Administration of Staphylococcal Enterotoxin B

Savransky

Rostapshov²,

Pinelis

et al. 2003

Toxicol Pathol

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Currently available murine staphylococcal enterotoxin B (SEB) shock models require pretreatment with various agents to increase mouse sensitivity to SEB. This study was performed to show that C3H/HeJ mice are highly susceptible to intranasal SEB inoculation, which caused toxic shock without using pretreatment agents. For this purpose, mice were injected intranasally with different doses of SEB and observed for up to 1 month. The median lethal dose of SEB was determined using the probit procedure. Tissue samples were taken at different time points for histopathological examination. The LD 50 was found at 1.6 µg/g (95% fiducial limit (f.l.) 0.7 to 2.2), the LD 80 at 2.7 µg/g (95% f.l. 1.9 to 4.0) and the LD 90 at 3.6 µg/g (95% f.l. 2.7 to 6.4). Histopathologic examination revealed pulmonary edema and bronchopneumonia. Mucosal-associated lymphoid tissue first became activated, followed by increasing lymphocyte apoptosis and depletion. In the liver there were intralobular and portal inflammatory foci with increasing lymphocyte apoptosis and degenerative necrosis. The splenic white pulp was characterized by early activation and subsequent depletion of lymphoid follicle germinal centers. The thymus initially was activated, followed by increasing apoptosis and migration of lymphoid cells from the cortex to the medulla. The pathological features detected in the mice were similar to those of rhesus monkeys treated with SEB aerosol challenge.

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Tumor necrosis factor-induced apoptosis during the poisoning of mice with hepatotoxins

Abstract: Hepatotoxins such as alpha-amanitin may induce liver failure by an indirect mechanism involving sensitization of parenchymal cells toward endogenously produced TNF.

Cited by 194 publications

References 61 publications

Evaluation and comparison of alpha- and beta-amanitin toxicity on MCF-7 cell line

Evaluation and comparison of alpha- and beta-amanitin toxicity on MCF-7 cell line

Energy supply and the shape of death in neurons and lymphoid cells

Murine Lethal Toxic Shock Caused by Intranasal Administration of Staphylococcal Enterotoxin B

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