The effects of nano-TiO2 (rutile) on the photochemical reaction of chloroplasts of spinach were studied. The results showed that when spinach was treated with 0.25% nano-TiO2, the Hill reaction, such as the reduction rate of FeCy, and the rate of evolution oxygen of chloroplasts was accelerated and noncyclic photophosphorylation (nc-PSP) activity of chloroplasts was higher than cyclic photophosphorylation (c-PSP) activity, the chloroplast coupling was improved and activities of Mg2+-ATPase and chloroplast coupling factor I (CF1)-ATPase on the thylakoid membranes were obviously activated. It suggested that photosynthesis promoted by nano-TiO2 might be related to activation of photochemical reaction of chloroplasts of spinach.

The effects of nano-TiO2 (rutile) on the chloroplast aging of spinach under light were studied. The results showed that when the chloroplasts were illuminated for 1, 5, and 10 min with 500 micromol/cm2/min light intensity, respectively, the evolution oxygen rate was rapidly increased; when the chloroplasts were treated for 20, 30, and 40 min with 500 micromol/cm2/min light intensity, respectively, the evolution oxygen rate was gradually decreased. While spinach was treated with 0.25% nano-TiO2, the rate of evolution oxygen of chloroplasts in different illumination times (1, 5, 10, 20, 30, and 40 min) was higher than that of control, and when the illumination time was over 10 min, the reduction of the evolution oxygen rate was lower than that of control. It suggested that nano-TiO2 treatment could protect chloroplasts from aging for long-time illumination. The mechanism researches indicated that nano-TiO2 treatment could significantly increase the activities of superoxide dismutase (SOD), catalase (CAT), and peroxidase (POD), decrease accumulation of reactive oxygen free radicals and the level of malondialdehyde (MDA), and maintain stability of membrane structure of chloroplast under light.

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Apoptosis of cardiomyocytes plays an important role in the development of cardiovascular diseases (CVD). Numerous studies have shown that generation of reactive oxygen species (ROS) induced by the renin-angiotensin system (RAS) is involved in this pathological process. Recent studies also suggested that acetylcholine (ACh) prevented the hypoxia-induced apoptosis of mouse ES cells by inhibiting the ROS production. However, whether ACh can inhibit the action of angiotensin II (Ang II) and subsequently prevent CVD development remains unclear. In this study, H9c2 cells were stimulated by 10(-6) M Ang II for 24 h with or without 10(-5) M ACh, 10(-5) M ACh + 10(-4) M atropine respectively. The results demonstrated that Ang II increased apoptosis index by fourfold (vs. the control group, P < 0.01), which were significantly diminished by ACh. However, the atropine (ACh receptor [AChR] inhibitor) treatment blocked the protective effect of ACh. Subsequently, Ang II significantly increases the expression and activity of NADPH oxidase so that ROS production is increased by sevenfold (vs. control group, P < 0.01). The activity and expression of caspase-3 along with the Bax/Bcl2 ratio and the levels of p38 mitogen activated protein kinase (MAPK) phosphorylation also appeared to follow a similar trend. Furthermore, we observed that ACh could reduce up-regulation of AT1 receptor expression induced by Ang II. However, all these effects of ACh were inhibited by atropine. In conclusion, ACh prevents Ang II-induced H9c2 cells apoptosis through down-regulation of the AT1 receptor and inhibition of ROS-mediated p38 MAPK activation as well as regulation of Bcl-2, Bax and caspase-3.