nase enzyme of S. brevidens that produces tomatidine from the precursor teinamine by hydrogenation of the double bond at position 5 also produces demissidine by hydrogenating the corresponding double bond in solanidine, a compound that is found in S. tuberosum but not in S. brevidens.
Celery is another example of where conventional plant breeding methods produced an unwanted result. Furanocoumarins are bioactive components of celery and are known to interact with DNA, are mutagenic and carcinogenic, are reproductive toxicants and cause contact dermatitis in humans. A celery line with resistance to Fusarium, but with concentrations of linear furanocoumarins high enough to cause severe contact dermatitis in field workers, was almost released for commercialization (Diawara and Trumble 1997; Trumble et al. 1990 and in press).
Transgenic pest-protected varieties commercialized to date in the United States have not been shown to have elevated levels of certain toxic compounds. For discussion during FDA consultation, companies monitor for changes in the levels of certain endogenous plant compounds. For example, ringspot-resistant transgenic pest-protected papaya lines were shown by chemical analysis to have no more of the suspected human toxicant benzyl isothiocyanate than nontransgenic varieties (University of Hawaii 1997).
The “edible” part of a plant varies with the species and the consumer in question. In the human diet, the part eaten can also vary with the cultural background of the consumer. Overall increases in the concentrations of secondary plant chemicals in the total plant might cause toxic chemicals that are normally present only in trace amounts in edible parts to be increased to the point where they pose a toxic hazard. In some cases, genes transferred by conventional breeding can also change the distribution of secondary plant compounds among plant parts. For example, cucumber was bred to produce a bitter protective compound, cucurbitacin, in the leaves and stems of the plant but not in the fruits. A single gene controls the restriction of the compound to the leaves and stems (Barham 1953).
Some plants cause either contact allergic responses or food allergies. However, only a few documented examples involving contact allergens-