the release of cytochrome c and reactive oxygen species. Release of cytochrome c from the mitochondria induces apoptosis by initiating the assembly of caspases, or proteins responsible for degrading the cell from within. Additionally, trichothecenes such as T-2, have also been shown to increase the c-Jun N-Terminal Kinase signaling pathway in cells. Here, c-Jun N-Terminal Kinase is able to increase to phosphorylation of its target, c-Jun, into its active form. Activated c-jun acts as a transcription factor in the cell nucleus for proteins important for facilitating the downstream apoptotic pathway. Symptomology The trichothecene mycotoxins are toxic to humans, other mammals, birds, fish, a variety of invertebrates, plants, and eukaryotic cells. The specific toxicity varies depending on the particular toxin and animal species, however the route of administration plays a significantly higher role in determining lethality. The effects of poisoning will depend on the concentration of exposure, length of time and way the person is exposed. A highly concentrated solution or large amount of the gaseous form of the toxin is more likely to cause severe effects, including death. Upon consumption, the toxin inhibits ribosomal protein, DNA and RNA synthesis, mitochondrial functions cell division while simultaneously activating a cellular stress response named ribotoxic stress response. The trichothecene mycotoxins can be absorbed though topical, oral and inhalational routes and are highly toxic at the sub-cellular, cellular, and organic system level. Trichothecenes differ from most other potential weapon toxins since they can act through the skin, which is attributed to their amphipathic and lipophilic characteristics. The small amphipathic nature of trichothecenes allows them to easily cross cell membranes and interact with different organelles such as the mitochondria, endoplasmic reticulum (ER). and chloroplast The lipophilic nature of trichothecenes allow them to be easily absorbed through skin pulmonary mucosa, and gut. Direct dermal application or oral ingestion of trichothecene causes rapid irritation to the skin or intestinal mucosa. As a dermal irritant and blistering agent, it is alleged to be 400 times more intoxicating than sulfur mustard. The response in the body to the mycotoxin, alimentary toxic aleukia, occurs several days after consumption, in four stages: The first stage includes inflammation of the gastric and intestinal mucosa. The second stage is characterized by leukopenia, granulopenia, and progressive lymphocytosis. The third stage is characterized by the appearance of a red rash on the skin of the body, as well as hemorrhage of the skin and mucosa.