Effects of cadmium and chlordane on cellular apoptosis in ecotoxicological test species

Cadmium and chlordane are compounds chosen for a preliminary study on the impact of environmental contaminants on apoptosis in different representative species. These two potentially toxic substances decrease in vitro apoptosis of Daphnia magna cells. This appears to be related to the chemical concentrations and the time exposure. Cadmium was also directly introduced to the cell culture medium of Syrian hamster embryos (SHE) or indirectly via daphnids, which had firstly consumed algae contaminated with cadmium. A very sharp transfer of cadmium toxicity from algae to daphnids is noted and an inhibition of the apoptosis in SHE cells can be observed.     

大气PM2.5对巨噬细胞的毒性作用研究

以上海市工业区，交通区、郊区3个功能区的大气PM2.5粒子，对腹腔巨噬细胞进行染毒培养，台酚蓝染色测定细胞存活率，酵母菌吞噬实验测定其吞噬功能，流式细胞仪检测凋亡情况，结果显示，随大气PM2.5粒子浓度增加，巨噬细胞存活率和吞噬功能下降，巨噬细胞出现凋亡，其中交通区大气PM2.5染毒组的观察指标改变较明显，提示了大气PM2.5粒子对巨噬细胞具有细胞毒性，而交通区大气PM2.5粒子的毒性较大。     

微羹藻毒素诱导细胞凋亡的相关信号通路研究进展

细胞凋亡是微蓑藻毒素（Mycrocystins,MCs）发挥其毒性效应的关键所在,但其具体毒性作用机制目前尚未明确,有关MCs诱导细胞凋亡机制的研究仍然是当前的热点。已有研究表明,MCs诱导细胞凋亡是通过多条信号通路来转导的,各通路间互相联系,共同调节细胞凋亡。本文总结了近年来MCs诱导细胞凋亡的相关信号通路的研究进展,以期为全面阐述MCs诱导细胞凋亡的信号传导通路机制奠定基础。     

Oxidative stress, endothelial dysfunction and inflammatory response in rat heart to NO₂ inhalation exposure

Epidemiological studies suggest that NO₂ inhalation is associated with adverse effects on heart-related health, however, existing experimental data lack relevant evidences. In this study, a role for oxidative stress, endothelial dysfunction and inflammatory responses in the heart of rats treated with different concentrations of NO₂ (0, 5, 10 and 20 mg m⁻³) was investigated. Mild heart pathology occurred after 7-d exposure (6 h d⁻¹). Marked oxidative stress were induced as evaluated by reduction/induction of antioxidants (Cu/Zn-SOD, Mn-SOD and GPx) activity and increasing formation of MDA and PCO. Also, mRNA and protein biomarkers of vasoconstriction (ET-1, eNOS) and inflammation (TNF-α, IL-1β and ICAM-1) were up-regulated, and p53 mRNA expression, bax/bcl-2 ratio and the mean number of TUNEL-positive myocytes were increased as well. All the results implicate that NO₂ exerted injuries to mammals’ heart, and the damage mechanisms were possibly associated with oxidative stress, endothelial dysfunction and inflammation.