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Scientist Warns of Dangers of
Genetically Engineered Food

The Risks of GM Food
Professor David Schubert
Cellular Neurobiology Lab, Salk Institute for Biological Studies, San Diego,
USA
July 2002


As a cell biologist I am very much discouraged by the content of the
ongoing debate about introducing genetically modified (GM) plants into the
marketplace. While the voiced concerns usually center around irrational
emotional arguments on the one hand, and the erroneous concept that genetic
engineering is just like plant breeding on the other, I believe that the three
issues which should be of most concern on the basis of established science
receive little or no discussion.

These are:
1. that introducing the same gene into 2 different types of cells can produce
two very distinct protein molecules;

2. the recent observations that the introduction of any gene, be it from a
different or the same species, always significantly changes overall gene
expression and therefore the phenotype of the recipient cell; and

3. the possibility that enzymatic pathways introduced to synthesize small
molecules such as vitamins can interact with endogenous pathways to produce
novel molecules. The potential consequence of all of these perturbations
could be the production of biomolecules that are either toxic or carcinogenic,
and there is no a priori way of predicting the outcome.

I will give a few examples and then argue why GM food is not a safe
alternative.

In addition to their primary sequence of amino acids, the structure and
biological activity of proteins can be modified by the addition of molecules
such as phosphate, sulfate, sugars or lipids. The nature of these secondary
modifications is totally dependent upon the cell type in which they are
expressed. For example, if a protein involved in the cause of Alzheimer's
disease, the beta amyloid precursor protein, is expressed in liver cells it
contains covalently attached chondroitin sulfate carbohydrate, while the
identical gene expressed in brain nerve cells contains a much simpler sugar.
This is because each cell type expresses a unique repertoire of enzymes
capable of modifying proteins after they are synthesized. Once modified, the
biological activity of the molecule may be changed. In the case of the _
amyloid precursor protein, the adhesive properties of the cells are changed,
but there is, at our current state of knowledge, no way of knowing the
biological effects of these modifications.

The second concern is the potential for inducing the synthesis of poisonous
or toxic compounds following the introduction of a foreign gene. These
observations are clearly at odds with the individuals who imply that
everything is fine because they are simply introducing one gene. In fact, the
introduction of a single gene invariably alters the gene expression pattern of
the whole cell and each cell of the individual or plant responds differently.
One recently published example is the transfection of a receptor gene into
human cells. In this case, the gene was a closely related isoform of an
endogenously expressed gene. The pattern of gene expression was monitored
using gene chip technology, and the mRNA levels of 5% of the genes was
significantly upregulated or downregulated. Similarly, the simple
introduction of a bacterial enzyme used for growth selection of transfected
cells changes the expression of 3% of the genes. While these types of
unpredicted changes in gene expression are very real, they have not received
much attention outside the community of the DNA chip users. Furthermore, they
are not unexpected. The maintenance of a specific cell phenotype is a very
precise balancing act of gene regulation, and any perturbation is going to
change the overall patterns of gene expression. The problem, like that of
secondary modifications, is that there is currently no way to predict the
resultant changes in protein synthesis.

Third, the introduction of genes for a new enzymatic pathway into
plants could lead to the synthesis of totally novel or unexpected products via
the interaction with endogenous pathways. Some of the products could be
toxic. For example, retinoic acid (vitamin A) and derivatives of retinoic
acid are used in many signaling events that control mammalian development.
Since these compounds are soluble and work at ultralow concentrations, a GM
plant making vitamin A may also produce retinoic acid derivatives which act as
agonists or antagonists in these pathways, resulting in abnormal embryonic
development.

Given the fact that genetically modified plants are going to make proteins
in different amounts and perhaps totally new proteins than their parental
species, what are the potential outcomes? A worst case scenario could be that
an introduced bacterial toxin is modified to make it toxic to humans. Direct
toxicity may be rapidly detected once the product enters the marketplace, but
carcinogenic activity or toxicity caused by interaction with other foods would
take decades to detect, if ever. The same outcomes would be predicted for the
production of toxins or carcinogens via indirect changes in gene expression.

Finally, if the above problems are real, what can be done to address
these concerns? The issue of secondary modification could be addressed by
continual monitoring of the introduced gene product by mass spectroscopy. The
problem is that some secondary modifications, like phosphorylation or
sulfation can be lost during purification. However, the best, and to me the
only reasonable solution, is to require all genetically engineered plant
products for human consumption be tested for toxicity and carcinogenicity
before they are marketed. These safety criteria are required for many
chemicals and all drugs, and the magnitude of harm caused by a widely consumed
toxic food would be much greater than that of any single drug.

Professor David Schubert
Cellular Neurobiology Lab
The Salk Institute for Biological Studies
P.O. Box 85800
San Diego, CA 92186-5800
USA

Phone: (001) (858) 453-4100
Email: schubert@salk.edu


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