Near infrared light exposure is associated with increased mitochondrial membrane potential in retinal pigmented epithelial cells.

The goal of this study was to characterize the effect of near-infrared light exposure on mitochondrial membrane potential, in vitro. We focused on the retinal pigmented epithelial (RPE) cells due to our interest in the visual health of military airmen exposed to infrared light, which causes thermal damage to the retina. Within RPE cells, an irradiance of 1.6 mW cm-2 for 30 minutes, resulting in a total fluence of 2.88 J cm-2, induces resistance to cell death in retinal pigmented epithelial cells exposed to a 1-sec hazardous pulse of 2 µm laser radiation 1. Thus, we examined the impact of this exposure on mitochondrial membrane potential in RPE cells. To do this, the fluorescent molecule, tetramethylrhodamine ethyl ester (TMRE), was used to quantify mitochondrial membrane potential. TMRE is a cell permeant, positively-charged, red-orange dye that readily accumulates in active mitochondria due to their relative negative charge. Depolarized or inactive mitochondria have decreased membrane potential and fail to sequester TMRE. Data from our study show that RPE cells exposed to an irradiance of 1.6 mW cm-2 for 30 minutes demonstrate elevations in mitochondrial membrane potential. This is the expectation if NIR light exposure is associated with oxygen consumption, as shown in previously published studies. Thus, by focusing on the uptake of TMRE in mitochondria, our findings provide additional details regarding the mechanism underlying the effect of NIR and potentially PBM in RPE cells. These findings may also apply to other cell types and red and NIR light exposures.

A dynamic compartment model for xylem loading and long-distance transport of iron explains the effect of kanamycin on metal uptake in Arabidopsis.

Arabidopsis plants exposed to the antibiotic kanamycin (Kan) display altered metal homeostasis. Further, mutation of the WBC19 gene leads to increased sensitivity to kanamycin and changes in iron (Fe) and zinc (Zn) uptake. Here we propose a model that explain this surprising relationship between metal uptake and exposure to Kan. We first use knowledge about the metal uptake phenomenon to devise a transport and interaction diagram on which we base the construction of a dynamic compartment model. The model has three pathways for loading Fe and its chelators into the xylem. One pathway, involving an unknown transporter, loads Fe as a chelate with citrate (Ci) into the xylem. This transport step can be significantly inhibited by Kan. In parallel, FRD3 transports Ci into the xylem where it can chelate with free Fe. A third critical pathway involves WBC19, which transports metal-nicotianamine (NA), mainly as Fe-NA chelate, and possibly NA itself. To permit quantitative exploration and analysis, we use experimental time series data to parameterize this explanatory and predictive model. Its numerical analysis allows us to predict responses by a double mutant and explain the observed differences between data from wildtype, mutants and Kan inhibition experiments. Importantly, the model provides novel insights into metal homeostasis by permitting the reverse-engineering of mechanistic strategies with which the plant counteracts the effects of mutations and of the inhibition of iron transport by kanamycin.