Single-rooted soybean leaves were used to investigate the suppression of photosynthesis through end-product inhibition during acclimation to CO(2 )enrichment. The photosynthetic activity was greater in leaves cultured at a CO(2) partial pressure of 70 Pa (high-CO(2)) than that in the leaves cultured at 35 Pa CO(2) (control) during the initial exposure to CO(2) enrichment but then decreased rapidly with a large accumulation of starch, to well below the level of the control leaves. The response curve of photosynthesis (A) to the intercellular CO(2) concentration (Ci) in the high-CO(2) leaves cultured long-term exhibited a significantly low initial gradient. However, on exposure to darkness for 48 h, the initial gradient of the A to Ci curve and rate of photosynthesis were completely restored, and almost all of the accumulated starch was expended. The ribulose bisphosphate carboxylase (RuBPcase) content and activation ratio in the high-CO(2) leaves remained high and roughly constant during the experiment, and were unchanged by the exposure, while this enzyme was slightly inactivated or inhibited after long-term exposure to CO(2) enrichment. The lower rate of photosynthesis in the high-CO(2) leaves could be linearly increased to a rate approaching the control level by increasing the external atmospheric [CO(2)], which thereby compensated for a reduced CO(2) transfer diffusion from the intercellular space to the stroma in chloroplasts. It is consequently concluded that, during the acclimation to CO(2 )enrichment, the suppression of photosynthesis through end-product inhibition was mainly caused by a lowering of the carboxylation efficiency of RuBPcase due to hindrance of CO(2) diffusion from the intercellular space to the stroma in chloroplasts brought about by the large accumulation of starch.

-CYP3A4 is an important drug-metabolizing enzyme induced by various compounds causing drug-drug interactions. However, the molecular mechanism of CYP3A4 induction is not completely understood. CYP3A4 induction is caused by pregnane X receptor (PXR) through binding to some PXR binding elements. These elements comprise an everted repeat separated by six nucleotides in the promoter region and distal nuclear receptor binding element 1 (dNR-1) as well as the essential distal nuclear receptor binding element for CYP3A4 induction (eNR3A4) in the enhancer region of the CYP3A4 gene. Recently, we found that polycyclic aromatic hydrocarbons including anthracene induce CYP3A4 in HepG2 cells with a different induction profile from that of rifampicin (RF), a typical PXR ligand. When a CYP3A4 reporter plasmid in which the eNR3A4 DNA fragment binds directly to the CYP3A4 promoter (-362 bases) was evaluated in a reporter assay, dibenz [a,h]anthracene (DBA) induced reporter activity, while RF did not. To be induced reporter activity by RF, more 14 nucleotides 5′ upstream of the eNR3A4 (rifampicin eNR3A4: reNR3A4) DNA fragment were required. However, eNR3A4 and reNR3A4 did not respond to recombinant PXR without dNR-1. These results suggest that eNR3A4 and reNR3A4 are necessary for CYP3A4 induction by DBA and RF, respectively, and that dNR-1 is indispensable for full induction through PXR.