Vitamins E and C reduce oxidative stress and mitochondrial permeability transition caused by camptothecin – an in vitro study

Camptothecin (CPT), a broad spectrum antineoplastic agent, is known to induce oxidative stress and mitochondria are among the main sources of intracellular reactive oxygen species (ROS). We investigated the merit of vitamins E and C supplementation on CPT-induced mitochondrial alterations in vitro. Following treatment of isolated liver mitochondria with CPT, we assessed the mitochondrial membrane permeability transition (MPT), concentration of malondialdehyde, antioxidants and activities of the enzymes of the respiratory chain and Krebs cycle. Our results provide evidence that CPT caused mitochondrial swelling, increased lipid peroxidation and transition of mitochondrial permeability. The CPT lowered the levels of reduced mitochondrial thiols suggesting that thiol oxidation is the mechanism underlying CPT-induced MPT. Identical experiments were also performed after preincubating the mitochondria with vitamins E and C. It was found that vitamins E and C pretreatment inhibited the deleterious effects of CPT and loss of enzyme activity was restored by antioxidant supplementation. Our results suggest that the toxicity of CPT was mediated by an increase in ROS production by mitochondria. However, the addition of vitamins E or C ameliorated the oxidative stress. We propose that an attempt to counteract the deleterious consequences of chemotherapy with nutritional therapies may be a rational approach in superior patient care especially in a disease like cancer.     

Toxicity of cigarette smoke on isolated lung,heart, and brain mitochondria: induction of oxidative stress and cytochrome c release

Cigarette smoking is one of the main risk factors for premature human death which is associated with a variety of respiratory and vascular diseases, and cancer due to exposure to hundreds of toxicants. Rat mitochondria were obtained by differential ultracentrifugation and incubated with different concentrations (1%, 10%, or 100%) of standardized cigarette smoke extract (CSE). Our results showed that CSE induced a rise in mitochondrial reactive oxygen species (ROS) formation, lipid peroxidation, and mitochondrial membrane potential (MMP) collapse before mitochondrial swelling ensued in isolated pulmonary mitochondria. Disturbance in oxidative phosphorylation was also confirmed by decrease in ATP concentration in the CSE-treated mitochondria. In addition, collapse of MMP and mitochondrial swelling produced release of cytochrome c via outer membrane rupture or mitochondrial permeability transition (MPT) pore opening. Our results suggested that CSE-induced toxicity in lung tissue is the result of disruptive effect on mitochondrial respiratory chain that leads to ROS formation, lipid peroxidation, MMP decline, and cytochrome c expulsion which results in apoptosis signaling and cell loss.     

Passive sampling of PAHs in indoor air in Nepal

PAHs were sampled in ten homes in the Makwanpur region, Nepal. SPMDs and moss bags (Sphagnum girgensohnii) were used as passive samplers. Soot particles on the SPMD surfaces were also analyzed for PAHs. The overall PAH concentrations in SPMDs were significantly higher than those in moss bags. Total PAH mean concentrations of ten houses were 535μg/g lipid for SPMDs and 7.2 μg/g moss (dw) for moss bags. Ratios of phenanthrene/anthracene in indoor SPMDs and particulate matter varied from 2.9 to 3.5 and ratios of fluoranthene/pyrene varied from 1.1 to 1.4. The values for moss bags were respectively 1.7–3.6 and 0.8–2.4. These ratios indicate that the PAHs are from combustion origin. The PAH concentrations in ambient air were estimated as B(a)P TEQs and they were 17–64 times higher than acceptable limit for Finnish community air. Based on PAH levels in the gas phase (SPMD) we may expect PAHs to have an impact on respiratory disease prevalence in Nepalese villages. Both of the sampling methods were feasible in the difficult conditions under which the study was performed.     

Effects of ellagic acid on arylamine N‐acetyltransferase activity in human colon tumor cells

The inhibition of arylamine N‐acetyltransferase (NAT) activity by ellagic acid was determined in a human colon tumor (adenocarcinoma) cell line. Two assay systems were performed, one with cellular cytosols (9000g supernatant), the other with intact colon tumor cell suspensions. The NAT activity in a human colon tumor cell line was inhibited by ellagic acid in a dose‐dependent manner in both types of examined systems: i.e. the greater the concentration of ellagic acid in the reaction, the greater the inhibition of NAT activities in both systems. The data also indicated that ellagic acid decreased the apparent K _m and V _max of NAT enzymes from human colon tumor cells in both the systems examined. This report is the first demonstration which showed ellagic acid affect human colon tumor cell NAT activity.     

鲨鱼皮微复制技术在抗菌防护领域中的应用研究

生物制造工程是在生命科学和仿生学基础上建立起来的前沿科技,通过基因复制、生物去除、生物生长、生物约束等方法将生物体特质直接复制到模具上,从而赋予产品特定的使用功能。本文通过对鲨鱼皮肤的分析论述了其抗菌机理以及利用生物约束成型技术将新鲜鲨鱼皮微结构复制到模具上的工艺流程。     

Avian Mortality at Oil Pits in the United States: A Review of the Problem and Efforts for Its Solution

Oil production operations produce waste fluids that may be stored in pits, open tanks, and other sites accessible to wildlife. Birds visit these fluid-filled pits and tanks (“oil pits”), which often resemble water sources, and may become trapped and die. The US Fish and Wildlife Service (USFWS) has a program to reduce these impacts by locating problem pits, documenting mortality of protected wildlife species, and seeking cleanup or corrective action at problem pits with the help of state and federal agencies regulating the oil industry. Species identification and verification of protected status for birds recovered from oil pits are performed at the USFWS National Fish and Wildlife Forensics Laboratory. From 1992 to 2005, a minimum of 2060 individual birds were identified from remains recovered from oil pits, representing 172 species from 44 families. The taxonomic and ecological diversity of these birds indicates that oil pits pose a threat to virtually all species of birds that encounter them. Ninety-two percent of identified bird remains belonged to protected species. Most remains identified at the Forensics Laboratory were from passerines, particularly ground-foraging species. Based on Forensics Laboratory and USFWS field data, oil pits currently cause the deaths of 500,000–1 million birds per year. Although law enforcement and industry efforts have produced genuine progress on this issue, oil pits remain a significant source of mortality for birds in the United States.     

氮沉降下西南亚高山针叶林生长的养分限制特征

长期氮(N)沉降及其诱导的N、磷(P)养分平衡性对森林生长与生产力的生态反馈效应已成为当前森林生态学研究的前沿与热点,但目前大多研究主要基于已有文献数据整合分析,而缺乏野外原位系统性研究与试验证据.以西南亚高山两种典型人工针叶林——云杉(Picea asperata)林和华山松(Pinus armandii)林为对象,...     

江苏启东邻近海域氮磷营养盐分布特征、组成及营养水平评价

基于江苏启东邻近海域2019年4月 、10月海水的调查数据,探讨该海域溶解无机氮(DIN)、溶解无机磷(DIP)的分布特征及成因,分析氮磷营养盐的构成特点,评价该海域的营养水平,通过DIN、DIP与环境因子的相关性分析,探讨影响DIN和DIP的主要环境因素.结果表明,春季各监测站位DIN、DIP平均质量浓度分别为0.3...     

环境监测优化布点的人工神经网络模型

采用B－P算法的人工神经网络,对选定的标准样本进行训练,用训练结束后网络的稳定权值和阈值,并结合标准样本的网络输出,即可对环境监测样点进行优选。应用于大气环境监测优化布点的实例结果表明,人工神经网络用于环境监测优化布点是可行的     

EROD activity and stable isotopes in seabirds to disentangle marine food web contamination after the Prestige oil spill

In this study, we measured via surgical sampling hepatic EROD activity in yellow-legged gulls from oiled and unoiled colonies, 17 months after the Prestige oil spill. We also analyzed stable isotope composition in feathers of the biopsied gulls, in an attempt to monitor oil incorporation into marine food web. We found that yellow-legged gulls in oiled colonies were being exposed to remnant oil as shown by hepatic EROD activity levels. EROD activity was related to feeding habits of individual gulls with apparent consequences on delayed lethality. Capture-recapture analysis of biopsied gulls suggests that the surgery technique did not affect gull survival, giving support to this technique as a monitoring tool for oil exposure assessment. Our study highlights the combination of different veterinary, toxicological and ecological methodologies as a useful approach for the monitoring of exposure to remnant oil after a large oil spill.