Apoptosis in Respiratory Epithelial Cells: Triggering by Paraquat and Modulation by L-ascorbic acid

PURPOSE: Apoptosis is a programmed cell death that is a selective process of physiological cell deletion. This study was undertaken to evaluate a paraquat-triggered apoptosis and the ability of ascorbic acid to modulate the process in the A549 cell line, a well-characterized cellular model of human lung alveolar cells. METHODS: A 549 cells were incubated with different concentrations of paraquat for up to 24 hour, followed by 24, 48, and 72 hours of recovery in paraquat-free medium. To test the abilities of antioxidants as modulators of paraquatinduced apoptosis, we pre-treated the cells for 4 hours with 250 micrometer L-ascorbic acid (vitamin C) before exposure to paraquat, and we incubated cells with paraquat in the presence of 250 micrometer L-ascorbic acid. Apoptosis was assayed by staining the cells with FITC-annexin V, and the cells were analyzed by using flow cytometry. RESULTS: Paraquat was inducer of apoptosis. A549 cells incubated with paraquat for up to 24 hour showed no apoptotic features, but the following incubation in a paraquat-free medium resulted in a time-dependent appearance of apoptosis. The ascorbic acid proved effective in reducing paraquat-induced apoptosis. CONCLUSION: We propose an experimental model for investigating the steps and mechanism of paraquat-induced apoptosis in alveolar cells

Clinical Analysis of Delayed Intracranial Hemorrhage in Head Injury

Experinece in the management of 74 patients with delayed traumatic intracranial hemorrhage(DTICH) of 474 head injury from January 1996 to December 1996 is poresented with emphasis on the incidence, occurring time, risk factors and outcome. The incidence of DTICH was 15.6% of all hospitalized head-injury patients. After an injury, every patient had an immediate computerized tomography(CT) scan to diagnose intracranial pathology and then CT follow-up was carried out according to intial CT finding and reurological deficit. The lesion was almost occurred in patients with initial abnormal CT finding(85.1%). 82.4% of DTICH were noted within 72 hours after injury. The delayed epidural hematoma and intracerebral hemorrhage were almost noted in first 72 hours(>90%), but the delayed subdural hemorrhage was found after a time interval varying from 6 hours to 10 days. So we strongly recommend CT follow-up in 4-8hour, 24-72hour, and then 7th day after head injury, especially in patients with initial abnormal CT findings. The risk factor of the delayed lesion was not hypotension, hypoxia, and consciousness level, but age of patients and the initial CT finding. The development of DTICH was not heralded by neurological deterioration. The prognosis of DTICH was not worse than non-DTICH. The patient with delayed subdural hemorrhage was better than the patient with non-delayed lesion(including hemorrhage and normal CT finding).