Copper iodide (CuI) thin film grown by a direct vacuum thermal evaporation method at low temperature is utilized as inorganic hole transport layer in planar CH 3 NH 3 PbI 3−x Cl x -based perovskite solar cell. The device performance is mainly controlled by the deposition rate of CuI layer for optimized thickness. The reason was investigated in detail by transient photovoltage/photocurrent spectroscopy (TPV/TPC), X-ray photoelectron spectroscopy (XPS), and the energy-dispersive X-ray spectrum (EDS). The results indicate that larger deposition rate leads to a non-stoichiometric CuI layer with excess iodine. More importantly, the redundant iodine is illustrated as the recombination center that results in interface recombination. Under optimized CuI growth condition, a power conversion efficiency of 6.4% has been achieved with a short-circuit current density (J SC ) of 16.4 mA/cm 2 , an open-circuit voltage (V OC ) of 730 mV, and a fill factor (FF) of 54%. Our results open a possibility for further improvement of perovskite solar cells by controlling the concentration and distribution of iodine in the perovskite films.
Iodine excess (IE) can cause thyroid dysfunction, thyroid diseases can adversely affect cardiovascular function. Accordingly, this study was to explore the direct and indirect effects of IE on endothelial function. Nthy-ori 3-1 and HUVECs cells were treated with potassium iodide (KI). CCK-8, LDH leakage, Elisa, RT-PCR and Western blotting were used to detect relevant indicators. Results showed that a certain level of KI can directly and indirectly reduce the viability of HUVECs and increase cytotoxicity. KI decreased the expression of ET-1 and VWF in HUVECs, inhibited the secretion of ET-1 in culture medium, and increased the expression of IL-6 and TNFα in HUVECs or Nthy-ori 3-1 cells alone. In the co-culture system, KI decreased the expression of ET-1 and THBD and increased the expression of TNFα and IL-6. Collectively, IE can directly and indirectly inhibit endothelial function of endothelial cells, which may be related to its induced inflammatory response.