[Effects on DNA damage and apoptosis and p53 protein expression induced by fluoride in human embryo hepatocytes].

OBJECTIVE: To study the effects of DNA damage and apoptosis and p53 expression, and to explore the relationship between apoptosis and p53 expression in human embryo hepatocytes induced by fluoride. METHODS: The rate of DNA damage, apoptosis and the level of p53 expression were investigated after the cells were incubated with sodium fluoride for about 24 hours. The concentrations of sodium fluoride of the control, A, B and C group were 0 microg/ml, 40 microg/ ml, 80 microg/ml and 160 microg/ml individually. RESULTS: The rate of DNA damage of every group treated with sodium fluoride were significantly higher than the control group (P < 0.05). The percentage of apoptosis of B and C groups increased apparently (P < 0.05). The level of p53 expression of B and C groups were significantly higher than the control group (P < 0.01). CONCLUSION: Fluoride can increase the rate of DNA damage, and induce apoptosis and expression of p53 in human embryo hepatocytes. Furthermore, both apoptosis and the level of p53 expression, there exists a rise tendency with the increase concentration of fluoride.

Effects of fluoride on lipid peroxidation, DNA damage and apoptosis in human embryo hepatocytes.

OBJECTIVE: To investigate the effects of fluoride on lipid peroxidation, DNA damage and apoptosis in human embryo hepatocyte L-02 cells. METHODS: Lipid peroxide (LPO) level, reduced glutathione (GSH) content, DNA damage, apoptosis, and cell cycle analysis were measured after in vitro cultured L-02 cells were exposed to sodium fluoride at different doses (40 microg/mL, 80 microg/mL, and 160 microg/mL) for 24 hours. RESULTS: Fluoride caused an increase of LPO levels and a decrease of GSH content in L-02 cells. There appeared to be an obvious dose-effect relationship between the fluoride concentration and the observed changes. Fluoride also caused DNA damage and apoptosis and increased the cell number in S phase of cell cycle in the cells tested. There was a statistically significant difference in DNA damage and apoptosis when comparing the high dose of fluoride treated cells with the low dose of fluoride treated cells. CONCLUSION: Fluoride can cause lipid peroxidation, DNA damage, and apoptosis in the L-02 cell experimental model and there is a significant positive correlation between fluoride concentration and these pathological changes.

[Study on the injury effect of ammonium perchlorate to lung].

OBJECTIVE: To study the injury effect of ammonium perchlorate (AP) to lung and to explore whether AP can cause pulmonary fibrosis. METHODS: To detect the levels of cell counts, TNF-alpha, MDA, HYP and the synthesis of collagen in BALF or rat lung after a certain time when rats were injected AP by intratracheal instillation. RESULTS: AP could bring about acute lung damage and inflammatory reaction. The levels of TNF-alpha of different groups in different time were obviously higher than the normal control group(P < 0.05). AP could affect the levels of MDA, HYP and the synthesis of collagen. But it had no obviously pathological change of pulmonary fibrosis. CONCLUSION: There were acute injury effect about AP to lung, but this experiment could not make sure whether AP could cause pulmonary fibrosis.

[Analysis on pneumoconiosis characteristic and its prediction in one coal mine].

OBJECTIVE: We aimed to investigate the characteristic of pneumoconiosis on coal miners and provide scientific evidences for its prevention. METHODS: To analyze the data of pneumoconiosis from one coal mine with the historical study and to predict its development tendency by the grey model of GM (1,1). RESULTS: (1) The year of work experience of pneumoconiosis (stage I) was 19.9 years and the age of its diagnosis (stage I) was 51.4 years. There was an obvious tendency that they became longer with years' back-shift. (2) During near forty years, the progression rates of pneumoconiosis from stage I to II and II to III were 13.6% and 11.2%, and the mean time was 8.3 and 8.1 years, respectively. It was obvious that the progression rate decreased gradually and the span prolonged with years' back-shift. (3) The complication rate of pneumoconiosis with lung tuberculosis was 12.5% and it increased with the progression of pneumoconiosis. The rate in dead cases was significantly higher than that in live cases (P < 0.01). (4) The sequence of death causes was pneumoconiosis (20.0%), lung tuberculosis (18.3%), chronic cor pulmonale (17.9%), and pulmonary carcinoma (9.0%), et al. (5) It was predicted that there would be 28 new cases every year during 2001-2020 years and the accumulated numbers of pneumoconiosis would be 2854 cases in 2020, but with a downward trends in the prevalence of -1.7%. CONCLUSION: It was suggested that the prevalence of pneumoconiosis should decrease obviously. However, it still remains a challenge about the task of effectively preventing and curing it or its complication.

[Research progress on oxidative stress and apoptosis].

Many research findings revealed that oxidative stress may induce apoptosis. At present, the explanations for this phenomenon are: 1) ROS activated nuclear factor-KB and induction of the expression of nuclear factor-KB; 2) mitochondria-mediated cell apoptosis; 3) ROS mediated DNA damage and P53 activation; 4) ROS activated SAPK pathway to apoptosis. In this paper, the progress on oxidative stress and apoptosis was reviewed.