Nitrate reduces the negative effect of UV radiation on photosynthesis and pigmentation in Gracilaria tenuistipitata (Rhodophyta): the photoprotection role of mycosporine-like amino acids

Photoprotection of the agarophyte red alga Gracilaria tenuistipitata against ultraviolet radiation (UVR) was investigated in algae submitted for 1 week to photosynthetically active radiation (PAR, 260 mu mol photons m(-2) s(-1)) or PAR + UVR (UV-A, 8.13 W m(-2) and UV-B, 0.42 W m(-2)) under different nitrogen concentrations: 0, 0.1, and 0.5 mM of NO3-. Photosynthetic pigments decreased during the time of the experiment mainly under low nitrogen supply and UVR. Incubation under high nitrogen supply (0.5 mM) sustained the photosynthetic levels over time. In contrast, mycosporine-like amino acids (MAAs) increased up to eightfold in the presence of UVR and 0.5 mM NO3-. Under PAR + UVR, maximal quantum yield was positively correlated to MAA abundance, whereas under PAR no correlation was found. The photosynthetic yield of algae cultivated during seven days under PAR + UVR was less affected by a 30-min exposure of high UVR (16 W m(-2)) and fully recovered after transferring to low PAR irradiances, whereas algae kept under PAR were more affected by UV exposure and no full recovery was observed. Growth rates decreased after three days in the presence of UVR and under low nitrate supply. However, these rates were similar when compared with treatments of PAR and PAR + UVR after seven days, with the exception of samples in 0 mM NO3-, indicating that the acclimation after one week's exposure is related to nitrate supply. In conclusion, the lowest negative effect of UVR on photosynthesis and growth rate in high N-supply-grown algae could be explained by the stimulation of photoprotection mechanisms, such as accumulation of MAAs. Photostimulation of MAA accumulation by UVR under high N supply was observed in G. tenuistipitata even after 20 years in culture without the induction of this photomorphogenic light signal.

Effect of simvastatin in the autonomic system is dependent on the increased gain/sensitivity of the baroreceptors

A number of mechanisms have been proposed to explain the pleiotropic effect of statin therapy to reduce sympathetic outflow in cardiovascular disease. We tested the hypothesis that statin treatment could improve baroreflex gain-sensitivity triggered by morphological adaptations in the mechanoreceptor site, thus reducing sympathetic activity, regardless of arterial pressure (AP) level reduction. Male spontaneously hypertensive rats (SHR) were divided into control (SHR, n = 8) and SHR-simvastatin (5 mg/kg/day, for 7 days) (SHR-S, n = 8). After treatment, AP, baroreflex sensitivity (BRS) in response to AP-induced changes, aortic depressor nerve activity, and spectral analyses of pulse interval (PI) and AP variabilities were performed. Internal and external carotids were prepared for morphoquantitative evaluation. Although AP was similar between groups, sympathetic modulation, represented by the low frequency band of PI (SHR: 6.84 ± 3.19 vs. SHR-S: 2.41 ± 0.96 msec2) and from systolic AP variability (SHR: 3.95 ± 0.36 vs. SHR-S: 2.86 ± 0.18 mmHg2), were reduced in treated animals. In parallel, simvastatin induced an increase of 26% and 21% in the number of elastic lamellae as well as a decrease of 9% and 25% in the carotid thickness in both, external and internal carotid, respectively. Moreover, improved baroreceptor function (SHR: 0.78 ± 0.03 vs. SHR-S: 1.06 ± 0.04% mv/mmHg) was observed in addition to a 115% increase in aortic depressor nerve activity in SHR-S rats. Therefore, our data suggest that the reduction of sympathetic outflow in hypertension by simvastatin treatment may be triggered by structural changes in the carotid arteries and increased BRS in response to an improvement of the baroreceptors discharge and consequently of the afferent pathway of the baroreflex arch.