N-acetylcysteine counteracts oxidative stress and protects alveolar epithelial cells from lung contusion-induced apoptosis in rats with blunt chest trauma

The aim of this study was to investigate the protective effects of N-acetylcysteine (NAC) on peroxidative and apoptotic changes in the contused lungs of rats following blunt chest trauma. The rats were randomly divided into three groups: control, contusion, and contusion + NAC. All the rats, apart from those in the control group, performed moderate lung contusion. A daily intramuscular NAC injection (150 mg/kg) was given immediately following the blunt chest trauma and was continued for two additional days following cessation of the trauma. Samples of lung tissue were taken in order to evaluate the tissue malondialdehyde (MDA) level, histopathology, and epithelial cell apoptosis using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay and active caspase-3 immunostaining. In addition, we immunohistochemically evaluated the expression of surfactant protein D (SP-D) in the lung tissue. The blunt chest trauma-induced lung contusion resulted in severe histopathological injury, as well as an increase in the MDA level and in the number of cells identified on TUNEL assay together with active caspase-3 positive epithelial cells, but a decrease in the number of SP-D positive alveolar type 2 (AT-2) cells. NAC treatment effectively attenuated histopathologic, peroxidative, and apoptotic changes, as well as reducing alterations in SP-D expression in the lung tissue. These findings indicate that the beneficial effects of NAC administrated following blunt chest trauma is related to the regulation of oxidative stress and apoptosis.     

A Second Family with Nonsyndromic Sensorineural Hearing Loss Linked to Xp21.2: Refinement of the DFN4 Locus within DMD

X-linked inherited hearing impairment is a group of heterogeneous disorders accounting for less than 2% of hereditary hearing loss. DFN4, a sex-linked hearing impairment associated with profound sensorineural hearing loss, has been previously mapped to Xp21.2, a region containing the DMD locus. We have identified a family from Turkey with deafness in which the disease maps to and refines the DFN4 locus. In contrast to the previous family, the crossover points are entirely within the DMD locus. Two-point lod score analysis for the markers DXS 997, DXS 1214, and DXS 1219 showed a lod score of 2.59. 5′ and 3′ crossovers were between DMD 44 and DXS 1219 and between DXS 1214 and DXS 985, respectively, suggesting that DFN4 is either an allele of DMD or a mutation in a DMD nested gene. The restriction of the DFN4 locus to DMD suggests that dystrophin may play an important role in hearing.