OBJECTIVE: To observe the effects of N-acetyl-L-cysteine (L-NAC) protect hair cells in the rat cochlea from injury of exposure to styrene. METHOD: Seventeen adult Long Evans rats were used in present study. The animals were randomly assigned into test group (n=9) and control group (n=8). The animals were exposed to styrene by gavage at 400 mg/kg (2 g styrene was mixed with 1 ml olive oil). Test group animals received styrene exposure plus L-NAC 325 mg/kg (L-NAC was dissolved in physiological saline solution) by intraperitoneal injection. Treatment was performed once a day, 5 days per week for 3 weeks. Control group animals received the same volume of saline injection on an identical time schedule used for the test group. The auditory brainstem response (ABR) thresholds of both ears elicited with clicks were measured before and at the end of the 3-week styrene or styrene plus L-NAC treatment. After hearing was re-assessed, animals were sacrificed and cochleae were quickly removed from the skull. Following fixation, whole specimens comprising the basilar membrane with Corti's organ were separated from the modiolus. The organs of Corti were stained with propidium iodide (PI) and the TUNEL assay to visualize the morphologic viability of hair cell nuclei, FITC-labeled phalloidin, a F-actin intercalating fluorescent probe used to visualize the morphologic viability of cuticular plate and the stereocilia in the hair cells. Each organ of Corti was thoroughly examined using fluorescence microscopy. The numbers of damaged OHCs (apoptotic, necrotic and missing OHCs) were documented. RESULT: There was a statistically significant decrease in ABR threshold shift (P<0.05) in the styrene-plus-L-NAC treated animals. The average percentage of damaged OHCs in the styrene-treated animals was 28.3%. In contrast, the average percentage of OHC damage in the styrene-plus-L-NAC treated group was only 10.6% (P<0.01). The percentage of reduction in the number of apoptotic cells in styrene-plus-L-NAC treated group was 78% (P<0.01). However, the mean reduction of necrotic cells was only 23% (P>0.05). CONCLUSION The results indicate that the treatment with L-NAC may effectively protect against the styrene-induced hair cells damage and preferably reduce the number of apoptotic OHCs.
Acetylcysteine ; analogs & derivatives ; pharmacology ; Animals ; Antioxidants ; pharmacology ; Cochlea ; cytology ; drug effects ; Evoked Potentials, Auditory, Brain Stem ; Hair Cells, Auditory ; drug effects ; pathology ; Lysine ; analogs & derivatives ; pharmacology ; Rats ; Rats, Long-Evans ; Styrene ; adverse effects

Congenital heart disease (CHD) is the most common birth defect and one of the major causes of neonatal death, with an average prevalence of 9.4‰ worldwide. We reviewed recent epidemiological studies and found that exposure to air pollutants is associated with increased CHD risks, but the associations are inconsistent between exposure to air pollutants and different subtypes of CHD due to developmental and etiological heterogeneity among different subtypes of CHD. It has been reported that air pollutants are associated with increased risks of ventricular septal defect, patent ductus arteriosus, pulmonary stenosis, tetralogy of Fallot, and transposition of the great arteries. However, associations between maternal exposure to air pollutants and atrial septal defect (ASD) are contradictory, with significantly positive associations of inhalable particulate matter and nitrogen dioxide exposure, negative associations of fine particulate matter and carbon monoxide, and mixed associations of sulfur dioxide. Adverse effects of air pollutant on cardiac development cover a wide time window beyond 3-8 weeks during gestation; particulate matter and nitrogen oxide are more likely to affect fetal heart in early pregnancy, while the association strength of carbon monoxide shows a trough in early pregnancy, and sulfur dioxide and ozone affect cardiac health throughout pregnancy. In addition, we discussed the limitations of previous studies on the associations between maternal air pollutant exposure and CHD, and highlighted the application of precise assessment on exposure to air pollutants, the performance of prospective cohort studies and longitudinal studies, and the necessity of studies on CHD subtypes, in order to provide scientific evidence to control exposure to environmental pollutants and CHD occurrence.