ricin/necrosis

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Cross-talk between the pathways leading to the induction of apoptosis and the secretion of tumor necrosis factor-alpha in ricin-treated RAW 264.7 cells.

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Ricin induced apoptotic nuclear morphological changes in mouse macrophage cell line RAW264.7 cells at concentrations sufficient to cause severe protein synthesis inhibition. Ricin also induced the release of tumor necrosis factor-alpha (TNF-alpha) from this cell line in a dose-dependent manner but

The modulating effects of tumor necrosis factor alpha antibody on ricin-induced oxidative stress in mice.

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Previous studies in our laboratory have shown that the protein toxin ricin induces an oxidative stress in mice, resulting in increased urinary excretion of malondialdehyde (MDA), formaldehyde (FA), and acetone (ACON). Other toxicants have been shown to induce oxidative stress by macrophage

Ricin induces the production of tumour necrosis factor-alpha and interleukin-1 beta by human peripheral-blood mononuclear cells.

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Ricin induced the release of tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 beta by human peripheral-blood mononuclear cells in a dose- and time-dependent manner. The inhibition induced by ricin upon the phytohaemagglutinin (PHA)-driven lymphocyte proliferation was greater in cultures of

Lethal ricin intoxication in two adult dogs: toxicologic and histopathologic findings.

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Two adult dogs with the same owner were intoxicated by ingestion of fertilizer composed of residual plant material of the castor bean plant (Ricinus communis L.). Both dogs died within 2 and 3 days, respectively, after the first signs of vomiting and abundant hemorrhagic diarrhea. Toxicologic and

[Ricin--from a Bulgarian umbrella to an optional treatment of cancer].

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Ricin toxin, found in the bean of the castor plant, is one of the most toxic and easily produced plant toxin. It is composed of two polypeptide chains linked by a disulfide bond. The toxin irreversibly blocks protein synthesis. Oral intoxication is the most frequent mode of exposure, but direct

Saporin induces multiple death pathways in lymphoma cells with different intensity and timing as compared to ricin.

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Ribosome-inactivating protein (RIP)-containing immunotoxins are currently used in clinical trials as anti-tumour drugs, in particular against haematological malignancies. In cell killing-based therapies it is important to identify the death pathways induced by the cytotoxic agent. The purpose of

FOCAL OR INSULAR NECROSIS PRODUCED BY THE BACILLUS OF TUBERCULOSIS.

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1. It must be accepted from a comparison between the histological changes described in the focal necroses due to abrin and ricin, diphtheria, eclampsia, blood-serum intoxication, typhoid fever, lobar pneumonia and glanders, and those described here in three cases of tuberculosis, that the last are

Ultrastructure of rat lung following inhalation of ricin aerosol.

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Ricin is one of a group of structurally related plant lectins and is extracted from the seeds of the Castor Oil plant, Ricinus communis. Groups of rats were exposed to ricin aerosol by inhalation, total LCt1-11.21 mg.min.m-3 (an approximate LCt30 exposure) and examined, using transmission electron

Toxicity of ricin toxin A chain in rats.

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Ricin toxin A chain (RTA) is the cytotoxic component of the dimeric protein, ricin, one of the most potent and deadly plant toxins extracted from the seeds of Ricinus communis. RTA has been investigated as a potential candidate for cancer chemotherapy, in the form of immunotoxins, and as a method

A two-domain protein triggers heat shock pathway and necrosis pathway both in model plant and nematode.

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The entomopathogen Bacillus thuringiensis is equipped with multiple virulent factors. The genome sequence of B. thuringiensis YBT1520 revealed the presence of a two-domain protein named Nel which is composed of a necrosis-inducing phytophthora protein 1-like domain found in phytopathogens and a

Recent advances in the development of vaccines against ricin.

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Several promising subunit vaccines against ricin toxin (RT) have been developed during the last decade and are now being tested for safety and immunogenicity in humans and for efficacy in nonhuman primates. The incentive to develop a preventive vaccine as a countermeasure against RT use as a

Morphological changes of ricin toxin-induced apoptosis in human cervical cancer cells.

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The morphological changes of ricin-induced apoptosis in a human cervical cancer cell line were studied. To shed light on the mechanism of action of ricin toxin (RT) at the cellular level, we examined cell growth, apoptosis, changes of mitochondrial membrane potential (MMP) and cytochrome C

Reactive oxygen species involvement in ricin-induced thyroid toxicity in rat.

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Ricin is known to have diverse effects on the cells of different organs like liver, kidney, pancreas, intestines and parathyroid. Acute decrease in serum thyroid hormone level 24 h after ricin administration (1.5 micrograms/100 g) led us to suspect the toxic action of ricin on the thyroid. We

Overcoming tumor necrosis factor and drug resistance of human tumor cell lines by combination treatment with anti-Fas antibody and drugs or toxins.

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Monoclonal mouse anti-Fas antibody is directed against Fas antigen, a M(r) 36,000 encoded polypeptide that belongs to the family of cell surface proteins which includes nerve growth factor receptor, tumor necrosis factor (TNF) receptors, B-cell antigen CD40, and T-cell antigens OX40. Anti-Fas

Treatment of ricin A-chain-induced hepatotoxicity with liposome-encapsulated N-acetylcysteine.

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BACKGROUND The toxicity of ricin resides in the ricin A-chain (RTA) and is attributed to the inhibition of protein synthesis but inflammation and oxidative stress have also been implicated. RTA can independently enter cells producing comparable tissue injury and inflammation, although at much higher

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