This study guided by device evaluations was conducted to reveal the reasons for the loss of the photo-generated carriers in CIGS cells with the buffer based on In2S3 derivatives. Chemical bath deposited Inx(OOH,S)y films have been employed as a Cd-free buffer layers. When compared to solar cells with CdS buffer layer, the Cu0.9(In0.7,Ga0.3)Se2.1 (Eg = 1.18 eV) cells with the Inx(OOH,S)y buffer exhibited strong voltage-dependent carrier collection and poor spectral response above 500 nm, presumably, due to energy barrier at the junction. In order to improve the charge collection by upward shift of the conduction band minimum of CIGS absorber, Inx(OOH,S)y/Cu0.9(In0.55,Ga0.45)Se2.1 (Eg = 1.30 eV) solar cells were also fabricated and their spectral responses were examined. When compared to the Cu0.9(In0.7,Ga0.3)Se2.1 cells, the improved spectral response and voltage dependent carrier collection were obtained. Nevertheless, considerable loss in charge collection above 500 nm was still observed. The efficiency reached 9.3% while the Cu0.9(In0.7,Ga0.3)Se2.1 cell exhibited only the efficiency of 3.4%. Finally, CIGS (Eg = 1.18 eV) solar cells with n-ZnO/i-ZnO/Inx(OOH,S)y/CdS/CIGS and n-ZnO/i-ZnO/CdS/Inx(OOH,S)y/CIGS configurations were fabricated. The influence of the TCO/buffer interface on the device characteristics was also addressed by means of comparison between the characteristics of two cells employing different interfaces. A 13.0% efficient cell has been achieved from n-ZnO/i-ZnO/CdS/Inx(OOH,S)y/CIGS configuration. The obtained data suggested that the limitation of the device efficiency was mainly related to the i-ZnO/Inx(OOH,S)y interface. The experimental results provide the knowledge base for further optimization of the interface properties to form high-quality p-n junction in the CIGS solar cells employing the CBD In2S3 buffer layer.

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Overdose of the analgesic and anti-pyretic acetaminophen causes a potentially fatal hepatic necrosis due to a high toxicity and depletion of cellular defense mechanisms. In the present work, the potential hepatoprotective effect of the fruit extract of Paeonia anomala against acetaminophen induced cell damages was evaluated in cultured HepG2 cells and compared to the root extract. The fruit extract showed a potent protection against acetaminophen induced cell death, while the root extract showed a weak protection. Particularly, the pre-treatment of lower doses of the fruit extract, 10 μg/ mL and 20 μg/mL, significantly enhanced cell viability. The level of total glutathione in HepG2 cells treated with the fruit extract prior to the treatment of 40 mM acetaminophen was enhanced, however, the root extract failed for this activity. In addition, activities of quinone reductase, glutathione peroxidase and glutathione reductase were increased and protein levels of glutathione peroxidase 1 and superoxide dismutase 1 were enhanced in the cells treated with 10-20 μg/mL of the fruit extract. Furthermore, the protein level of Nrf2, a crucial regulator for detoxifying and antioxidant systems, was increased by the fruit extract treatment. These results suggest that the fruit extract of P. anomala exerts protective effects against acetaminophen-induced toxicity through activation of key antioxidant systems.DOI: http://dx.doi.org/10.5564/mjc.v14i0.190 Mongolian Journal of Chemistry 14 (40), 2013, p.5-11

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