This study examined the effects of water temperature and the origin (terrestrial vs marine) and light history of chromophoric dissolved organic matter (CDOM) on the apparent quantum yields of carbon monoxide (CO) photoproduction for water samples collected along a salinity gradient (salinity range: 0-33) in the St. Lawrence estuarine system (Canada). The solar insolation-weighted mean apparent quantum yield of CO (phico) decreased as much as fourfold with increasing salinity and showed a strong positive correlation with the dissolved organic carbon-specific absorption coefficient at 254 nm. This suggests that terrestrial CDOM is more efficient at photochemically producing CO than is marine algae-derived CDOM and that aromatic moieties are likely involved in this photoprocess. CDOM photobleaching, mainly at the very early stage, dramatically decreased phico (by up to 6.4 times) for low-salinity samples, but photobleaching had little effect on the most marine sample. For a 20 degree C increase in temperature, phico increased by approximately 70% for low-salinity samples and 30-40% for saline samples. This study demonstrates that water temperature, as well as the CDOM's origin and light history, strongly affect the efficiency of CO photoproduction. These factors should be taken into account in modeling the photochemical fluxes of CO and other related CDOM photoproducts on varying spatiotemporal scales.
Iron is essential for proliferation of normal and neoplastic cells. Cellular iron uptake, utilization and storage are regulated by transcriptional and post-transcriptional mechanisms. We hypothesized that the disruption of iron homeostasis may modulate the growth properties of cancer cells. To address this, we employed H1299 lung cancer cells engineered for tetracycline-inducible overexpression of the post-transcriptional regulator iron regulatory protein 1 (IRP1). The induction of IRP1 (wild-type or the constitutive IRP1(C437S) mutant) did not affect the proliferation of the cells in culture, and only modestly reduced their efficiency to form colonies in soft agar. However, IRP1 dramatically impaired the capacity of the cells to form solid tumor xenografts in nude mice. Tumors derived from IRP1-transfectants were <20% in size compared to those from parent cells. IRP1 coordinately controls the expression of transferrin receptor 1 (TfR1) and ferritin by binding to iron-responsive elements (IREs) within their mRNAs. Biochemical analysis revealed high expression of epitope-tagged IRP1 in tumor tissue, which was associated with a profound increase in IRE-binding activity. As expected, this response misregulated iron metabolism by increasing TfR1 levels. Surprisingly, IRP1 failed to suppress ferritin expression and did not affect the levels of the iron transporter ferroportin. Our results show that the overexpression of IRP1 is associated with an apparent tumor suppressor phenotype and provide a direct regulatory link between the IRE/IRP system and cancer.
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