Phytotoxins toxic effects

This toxic protein is contained in caster seeds but does not pass into the oil. Similar phytotoxins occur in croton seeds (Crotin) jequirity seeds (Abrin) the bark of the locust tree, Robinia pseudo-acacia (Robin) and in the seeds of some leguminous plants (Phasin). The last is but weakly toxic. Ricin is responsible for the toxic effects on eating castor seeds 5 or 6 of these are fatal to a child, 20 to adults, and 3 or 4 seeds may cause violent gastroenteritis with nausea, headache, persistent vomiting, colic, sometimes bloody diarrhea, thirst, emaciation, and great debility. The symptoms usually do not set in until after several days. More severe intoxications cause small frequent pulse, cold sweat, icterus, and convulsions. Death occurs in 6 to 8 d, from the convulsions or from exhaustion. The fatality rate is about 6%. This low fatality rate is due to the destruction of the poison in the alimentary canal. The treatment would be evacuant and symptomatic. Usually, 3 to 10 d are required to complete recovery. 

Inhibition of ceramide synthase could cause symptoms by depletion of ceramide and ceramide derivatives or by toxic increases in sphinganine and its derivatives. The effects of these phytotoxins are so rapid, that it is unlikely that depletion of ceramides is responsible for cellular death. Others have invoked induction of apoptosis in the mode of action of these compounds [e.g., 6] however, treatment of plant tissues with phytoshingosine and sphinganine causes symptoms very similar to those caused by inhibition of ceramide synthase [7]. Very low levels of AAL-toxin tuid other ceramide synthase inhibitiors may cause apoptosis, but the rapidity of plasma membrtme damage at one micromolar and higher concentrations makes it unlikely that it is involved in the main phytotoxic effect. Attempts have been made to find a ceramide synthase inhibitor with good phytotoxicity, but little mammalitm toxicity [e.g., 8]. However, even inhibitors with little structural similarity to the fumonisins such as australifimgin [9], have relatively little difference between mammalian and plant toxicity. Nevertheless, these studies demonstrate that the ceramide synthase pathway is a viable site for herbicides, provided an inhibitor can be found that is plant specific. This topic is considered in more detail in a recent review [10]. 

Symptoms of ceramide synthase inhibition could be caused by depletion of ceramide and ceramide derivatives or by toxic increases in sphinganine and its derivatives. The effects of these phytotoxins are so rapid, that it is unlikely that depletion of ceramides is responsible for cellular deatii. Others have invoked induction of apoptosis in die mode of action of these confounds (e.g., 9) however, treatment of plant tissues with phytosphingosine and sphinganine causes synq)toms very similar to tiiose caused by inhibition of ceramide synthase (JO). The very rapid plasma membrane damage at one micromolar and higher... 

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