Exposure to PM2.5 Enhances the PI3K/AKT Signaling and Malignancy of ERα Expression-dependent Non-small Cell Lung Carcinoma

Atmospheric particulate matter(PM)2.5 is a major carcinogen and is associated with an increased risk of developing various cancers and pulmonary fibrous diseases[1-2].Non-small cell lung cancer(NSCLC)is the major type of lung cancer with high morbidity and mortality rates.Epidemiological studies report that the incidence of NSCLC,particularly adenocarcinoma,significantly differs with the gender[3].Female patients with NSCLC have unique epidemiologic characteristics,imaging profiles,clinical manifestations,and pathological characteristics[4].

Endocrine Disruption Activity of 30-day Dietary Exposure to Decabromodiphenyl Ethane in Balb/C Mouse

Objective This study aimed to evaluate the hepatotoxicity, metabolic disturbance activity and endocrine disrupting activity of mice treated by Decabromodiphenyl ethane （DBDPE）. Methods In this study, Balb/C mice were treated orally by gavage with various doses of DBDPE. After 30 days of treatment, mice were sacrificed; blood, livers and thyroid glands were obtained, and hepatic microsomes were isolated. Biochemical parameters including 8 clinical chemistry parameters, blood glucose and hormone levels including insulin and thyroid hormone were assayed. The effects of DBDPE on hepatic cytochrome P450 （CYP） levels and activities and uridinediphosphate-glucuronosyltransferase （UDPGT） activities were investigated. Liver and thyroid glands were observed. Results There were no obvious signs of toxicity and no significant treatment effect on body weight, or liver-to-body weight ratios between treatment groups. The levels of ALT and AST of higher dose treatment groups were markedly increased. Blood glucose levels of treatment groups were higher than those of control group. There was also an induction in TSH, T3, and f T3. UDPGT, PROD, and EROD activities were found to have been increased significantly in the high dose group. Histopathologic liver changes were characterized by hepatocyte hypertrophy and cytoplasmic vacuolization. Our findings suggest that DBDPE can cause a certain degree of mouse liver damage and insufficiency. Conclusion DBDPE has the activity of endocrine disruptors in Bal/C mice, which may induce drug-metabolizing enzymes including CYPs and UDPGT, and interfere with thyroid hormone levels mediated by Ah R and CAR signaling pathways. Endocrine disrupting activity of DBDPE could also affect the glucose metabolism homeostasis.

Single Wall Carbon Nanotube Induced Inflammation in Cruor-Fibrinolysis System

Objective To study single wall carbon nanotubes （SWCNT） and its role in inducing inflammatory cytokines in the cruor-fibrinolysis system of rat. Methods Twenty one Wistar rats were divided into four groups： 1） control; 2） low-dose SWCNT （0.15 mg/kg BW）; 3） medium-dose SWCNT （0.75 mg/kg BW）; 4） high-dose SWCNT （1.5 mg/kg BW）. Intratracheal instillation of SWCNT suspensions was administered to rats once per day for 21 days. In order to assess the exposure effect of SWCNT to the rats, activity of Inflammatory cytokine was measured and markers of cruor-fibrinolysis system were studied via ELSIA. Also, change in clotting time was recorded and histopathology was studied. Results IL-6 and IL-8 concentrations of rats exposed to SWCNT were significantly higher than those in controls （P〈0.05）. The activity of inflammatory cytokines and histopathological change indicated that oxidative damage occurred. Change in clotting time in rats exposed to SWCNT decreased compared with controls. Meanwhile, t-PA （tissue-tupe plassminogen activator） and AT-Ⅲ （antithrombin-Ⅲ） levels in rats exposed to particulates increased or decreased significantly compared with controls （P〈0.05）. A similar trend was observed for D-dimer （D2D） levels, indicating that SWCNT can impact the cruor-fibrinolysis system ofrat. Conclusion The results from our study suggest that an increased procoagulant activity and reduced fibrinolytic activity in rats exposed to SWCNT can cause pulmonary oxidative stress and inflammation, due to the release of pro-thrombotic and inflammatory cytokines into the blood circulation of rat.