Cytotoxicity and genotoxicity of multi-walled carbon nanotubes with human ocular cells

Cytotoxicity and genotoxicity of plasma-modified multi-walled carbon nanotubes (MWCNTs), including hydroxyl-MWCNTs (MWCNT-OH), carboxyl-MWCNTs (MWCNT-COOH) and pristine MWCNTs, with human ocular cells (e.g. retinal pigment epithelium (RPE) cells) have been studied in this work. The addition of MWCNT-based materials caused few change in cell morphology while the presence of MWCNTs was observed inside the cells using transmission electron microscopy (TEM), suggesting possibility of MWCNTs passing through the cell membranes without damaging cells. Cell viability measurements suggested that MWCNT-COOH exhibited better biocompatibility than other MWCNT materials studied in this work. Lactate Dehydrogenase (LDH) release level was found to be less than 30% with all types of MWCNT-based materials. Reactive Oxygen Species (ROS) generation was visible but not severe with addition of nanotubes. A smaller oxidative stress level was obtained from MWCNT-COOH. Cell apoptosis was found to be less than 1.5% with addition of MWCNT-based materials. Particularly MWCNTs were found to be swallowed by cells and released by cells after 72 h without damaging cells, which may be considered as a potential vector for ocular genetic diseases. Plasma modification of MWCNTs particularly with-COOH was found to be an efficient way to improve ocular biocompatibility of MWCNTs, suggesting a fast and useful way to modify MWCNTs for applications in areas such as biology and biomedicine.     

中空介孔硅球对血管内皮细胞的细胞毒性

通过细胞增殖实验和乳酸脱氢酶释放实验,流式细胞术,透射电镜及电感耦合等离子体发射光谱仪检测等方法,证实HMSN在浓度超过62.5 μg/mL时,会对人脐静脉血管内皮细胞产生毒性,半抑制浓度约为150 μg/mL.高浓度下HMSN导致细胞增殖抑制和乳酸脱氢酶释放,使细胞周期阻滞在G1期,并最终诱导细胞坏死.同时发现HMS...     

Suppression of tumorigenicity in human colon carcinoma cells by introduction of normal chromosome 5 or 18.

Development of colon carcinomas can be associated with allelic deletions on several chromosomes, including 5q and 18q. The APC gene on 5q and the DCC gene on 18q have been identified as potential tumour suppressor genes, whose suppression contributes to colon carcinogenesis. To investigate the role of genes in these deleted regions, we have now introduced a single normal human chromosome into a human colon carcinoma cell line, COKFu, through microcell hybridization. Several clones of hybrid cells containing normal chromosome 5, and others containing normal chromosome 18, were obtained. The morphology of the hybrid cells was markedly altered: the hybrids with chromosome 5 exhibited a closely packed polygonal morphology, and the hybrid cells with chromosome 18 were flattened. The cloning efficiency of the hybrid cells in soft agar was reduced from 0.46 to 0% of that of the parental carcinoma cells, and the tumorigenicity of these hybrid cells in athymic nude mice was completely suppressed. The growth properties of the hybrid cells with chromosome 11 were not substantially changed. These results strongly suggest that the genes on normal chromosome 5 and 18 function as tumour suppressors in colon carcinogenesis.     

Amyloid beta-peptide is produced by cultured cells during normal metabolism.

Alzheimer's disease is characterized by the extracellular deposition in the brain and its blood vessels of insoluble aggregates of the amyloid beta-peptide (A beta), a fragment, of about 40 amino acids in length, of the integral membrane protein beta-amyloid precursor protein (beta-APP). The mechanism of extracellular accumulation of A beta in brain is unknown and no simple in vitro or in vivo model systems that produce extracellular A beta have been described. We report here the unexpected identification of the 4K (M(r) 4,000) A beta and a truncated form of A beta (approximately 3K) in media from cultures of primary cells and untransfected and beta-APP-transfected cell lines grown under normal conditions. These peptides were immunoprecipitated readily from culture medium by A beta-specific antibodies and their identities confirmed by sequencing. The concept that pathological processes are responsible for the production of A beta must not be reassessed in light of the observation that A beta is produced in soluble form in vitro and in vivo during normal cellular metabolism. Further, these findings provide the basis for using simple cell culture systems to identify drugs that block the formation or release of A beta, the primary protein constituent of the senile plaques of Alzheimer's disease.