NOTE: Turns out that beta-carotene (precursor to Vitamin A that's been engineered into golden rice) is processed into a number of compounds, not just Vitamin A.  Some of these compounds actually block the action of Vitamin A itself.

The scientists who did this study say it may have implications for golden rice: "A concern is that if you engineer these crops to have unusually high levels of beta-carotene, they might also have high levels of these [Vitamin A-blocking] compounds."
http://www.nutraingredients.com/Research/Researchers-reveal-dark-side-to-high-beta-carotene-intake

For our backgrounder on golden rice see:
http://gmwatch.org/gm-myths/11130
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Naturally Occurring Eccentric Cleavage Products of Provitamin A β-Carotene Function as Antagonists of Retinoic Acid Receptors
Abdulkerim Eroglu, Damian P. Hruszkewycz, Carlo dela Sena, Sureshbabu Narayanasamy, Ken M. Ried, Rachel E. Kopec”–, Steven J. Schwart, Robert W. Curley Jr. and Earl H. Harrison
The Journal of Biological Chemistry
http://www.jbc.org/content/287/19/15886.abstract

© 2012 by The American Society for Biochemistry and Molecular Biology

Abstract

β-Carotene is the major dietary source of provitamin A. Central cleavage of β-carotene catalyzed by β-carotene oxygenase 1 yields two molecules of retinaldehyde. Subsequent oxidation produces all-trans-retinoic acid (ATRA), which functions as a ligand for a family of nuclear transcription factors, the retinoic acid receptors (RARs). Eccentric cleavage of β-carotene at non-central double bonds is catalyzed by other enzymes and can also occur non-enzymatically. The products of these reactions are β-apocarotenals and β-apocarotenones, whose biological functions in mammals are unknown. We used reporter gene assays to show that none of the β-apocarotenoids significantly activated RARs. Importantly, however, β-apo-14”²-carotenal, β-apo-14”²-carotenoic acid, and β-apo-13-carotenone antagonized ATRA-induced transactivation of RARs. Competitive radioligand binding assays demonstrated that these putative RAR antagonists compete directly with retinoic acid for high affinity 
binding
to purified receptors. Molecular modeling studies confirmed that β-apo-13-carotenone can interact directly with the ligand binding site of the retinoid receptors. β-Apo-13-carotenone and the β-apo-14”²-carotenoids inhibited ATRA-induced expression of retinoid responsive genes in Hep G2 cells. Finally, we developed an LC/MS method and found 3 5 nM β-apo-13-carotenone was present in human plasma. These findings suggest that β-apocarotenoids function as naturally occurring retinoid antagonists. The antagonism of retinoid signaling by these metabolites may have implications for the activities of dietary β-carotene as a provitamin A and as a modulator of risk for cardiovascular disease and cancer.