The effects of benomyl and its breakdown products carbendazim and butyl isocyanate on the structure and function of tracheal ciliated cells

Abstract

The effects of the fungicide benomyl and its breakdown products, carbendazim and butyl isocyanate, were examined on canine tracheal epithelial tissue in primary culture. Changes in ciliary frequencies were monitored with an optical spectrum analysis system. Serial dilutions of the test compounds were prepared in 100% corn oil and applied to the cell cultures for intervals up to 6 hours and frequencies measured at intervals of 15 minutes to 1 hour. Benomyl and butyl isocyanate caused concentration‐dependent decreases in ciliary beat frequency. Benomyl at 300 μg/ml (3 mM) caused ciliostasis within 75 minutes of exposure. Butyl isocyanate at a molar concentration three times lower than benomyl (1 mM) caused a similar response, although within 30 minutes. The IBC₅₀ for benomyl was 0.75 mM, while for butyl isocyanate it was 0.52 mM. Carbendazim caused a moderate decrease in frequency over a 6 hour exposure period. Benomyl caused moderate to severe swelling of the mitochondria of ciliated epithelial cells with other cell organelles appearing normal. Butyl isocyanate did not cause any noticeable effect on cell ultrastructure and the apparently low rate of penetration of carbendazim into cells made it impossible to obtain an effect which justified ultrastructural analysis. It appears, at least for benomyl and butyl isocyanate, that while the physiological effect of these two compounds (inhibition of ciliary beat) is the same, the sites of action in the cell may be different.     

Effects of UV-A LED light irradiation on growth of cultured RAW 264.7 cells

The aim of this study was to examine the effects of ultraviolet A (UV-A) irradiation-induced damage on cultured macrophage RAW 264.7 cells and determine which components produced these manifestations. RAW 264.7 cells were irradiated with 365 nm UV-A using a light-emitting diode (LED). Cell viability and damage were determined using a calcein-AM and propidium iodide dual-staining assay and lactate dehydrogenase leakage, respectively. Intracellular reactive oxygen species (ROS) were measured by H₂DCF-DA. The components of ROS in each medium were measured using an electron paramagnetic resonance (EPR) spectrometer in the presence of 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) and 2,2,5,5-tetramethyl-3-pyrroline-3-carboxamide (TPC). While UV-A irradiation for 2 min significantly suppressed cell growth, LDH leakage did not occur. Addition of N-acetyl cysteine restored inhibition of cell proliferation, and reduced intracellular ROS levels. The EPR signal in the presence of TPC increased with time but was decreased by sodium azide. In addition, a typical EPR spectrum was obtained in the presence of DMPO, indicating the presence of a hydroxyradical. The spectrum was diminished by L-histidine. Data suggest that ROS generated in cells or culture medium by UV-A irradiation is predominantly singlet oxygen, and this singlet oxygen suppressed cell proliferation.     

Nanosilica exerts cytotoxicity and apoptotic response via oxidative stress in mouse embryonic fibroblasts

Nanoscale silica is an important industrial material and extensively used in medicines. The objective of this study was to determine potential cytotoxicity and genotoxic effects attributed to nanosilica exposure in mouse embryonic fibroblasts (L929) cells. Nanosilica produced mild cytotoxicity in L929 cells. Results showed that nanosilica increased thiobarbituric acid reactive substance levels and enhanced superoxide dismutase activity but decreased levels of glutathione. This was accompanied by a concomitant generation of reactive oxygen species, loss of mitochondrial membrane potential, and activation of caspase-3 activity. In addition, in the single-cell gel test, nanosilica (50–300 μg/ml) at two treatment times 24 and 48 hr produced concentration- and time-dependent increase of DNA damage. Therefore, the obtained results indicate that nanosilica may induce genotoxic effects in cultured L929 cells associated with induction of oxidative stress.     

Studying developmental neurotoxic effects of bisphenol A (BPA) using embryonic stem cells

There is little to no toxicity information regarding thousands of chemicals to which people are exposed daily. In fact, of the 84,000 chemicals listed in the United States Toxic Substances Control Act Inventory, there is limited information available on their effects on neural development (Betts, 2010 and US EPA, 2015). The number of chemicals tested remains low due to the high cost of conducting multi-generational animal studies and the lack of alternative testing methods.     

Assessment of Bisphenol A (BPA) neurotoxicity in vitro with mouse embryonic stem cells

The adverse effects of environmental pollution on our well-being have been intensively studied with many in vitro and in vivo systems. In our group, we focus on stem cell toxicology due to the multitude of embryonic stem cell (ESC) properties which can be exerted in toxicity assays. In fact, ESCs can differentiate in culture to mimic embryonic development in vivo, or specifically to virtually any kind of somatic cells. Here, we used the toxicant Bisphenol A (BPA), a chemical known as a hazard to infants and children, and showed that our stem cell toxicology system was able to efficiently recapitulate most of the toxic effects of BPA previously detected by in vitro system or animal tests. More precisely, we demonstrated that BPA affected the proper specification of germ layers during our in vitro mimicking of the embryonic development, as well as the establishment of neural ectoderm and neural progenitor cells.     

微生物燃料电池的研究综述

微生物燃料电池是一种利用微生物的催化作用,将燃料中的化学能转化为电能,同时又可以处理废水的新型技术,具有显著的环境效益和经济效益。本文对微生物燃料电池的基本原理进行了详细的叙述,对一些影响微生物燃料电池在处理污水时发电的基本因素做了较全面的比较,同时也探讨了一些现阶段微生物燃料电池的瓶颈问题。展望了微生物燃料电池(MFCs)这一绿色技术的良好的发展前景。     

Mitochondrial electron transport chain is involved in microcystin-RR induced tobacco BY-2 cells apoptosis

Microcystin-RR （MC-RR） has been suggested to induce apoptosis in tobacco BY-2 cells through mitochondrial dysfunction including the loss of mitochondrial membrane potential . TO further elucidate the mechanisms involved in MC-RR induced apoptosis in tobacco BY-2 cells, we have investigated the role of mitochondrial electron transport chain （ETC） as a potential source for reactive oxygen species （ROS）. Tobacco BY-2 cells after exposure to MC-RR （60 mg/L） displayed apoptotic changes in association with an increased production of ROS and loss of Am. All of these adverse effects were significantly attenuated by ETC inhibitors including Rotenone （2 μmol/L, complex I inhibitor） and antimycin A （0.01 μmol/L, complex III inhibitor）, but not by thenoyltrifluoroacetone （S μmol/L, complex Ⅱinhibitor）. These results suggest that rnitochondrial ETC plays a key role in mediating MC-RR induced apoptosis in tobacco BY-2 cells through an increased mitochondrial production of ROS.     

石油污染物对海底微生物燃料电池性能的影响及加速降解效应

海底石油污染物在缺氧环境下导致其生物降解过程缓慢,对海洋环境造成长期危害.本文利用海底微生物燃料电池(BMFCs)原理,尝试通过电催化作用提高海底石油污染物的降解速率.对比测试了含油电池装置(BMFCs-A)与无油电池装置(BMFCs-B)的电化学性能,研究了石油污染物对电池性能的影响;比较了含油通路(BMFCs-A)和断路状态下(BMFCs-C)的石油降解率和细菌聚集量,分析了BMFCs对石油污染物降解的加速作用.结果表明,BMFCs-A和BMFCs-B阳极的交换电流密度分别为1.37×10-2A·m-2和1.50×10-3A·m-2,最大输出功率密度分别是105.79 m W·m-2和83.60 m W·m-2,BMFCs-A装置的抗极化能力增强,交换电流密度提高近9倍,最大输出功率密度提高1.27倍.BMFCs-A和BMFCs-C阳极表面的异养菌数量分别是(66±3.61)×107CFU·g-1和(7.3±2.08)×107CFU·g-1,细菌数量增加了8倍,高的异养菌数量导致石油降解加速进行,BMFCs的石油降解率是自然条件下的18.7倍.BMFCs在电化学性能提高的同时,加速石油污染物的降解.本文同时提出了一种海底微生物燃料电池对石油污染物加速降解的新模式.     

酵母生物转化生产2-苯乙醇的研究进展

主要论述了利用酵母菌生物转化合成天然2苯乙醇的研究进展,从应用微生物学的角度介绍了2苯乙醇生产菌株的筛选,分析了2苯乙醇合成过程中几方面因素的影响和培养条件的选择,并对产物原位转移技术作了简要说明.并从分子生物学的角度出发,对生物转化的重点途径———艾利希途径在基因水平上作了诠释,且例举了利用从头合成途径进行的基因工程育种,旨在为利用微生物生产2苯乙醇的研究开发提供参考.图1参40