自由基机制在硫化氢中毒性肺损伤中的作用

Role of Free Radicals in Lung Damage after HydrogenSulfide Inhalation

本文观察了自由基机制在大鼠硫化氢吸入中毒肺损伤中的作用。测定了肺组织及支气管肺泡灌洗液中丙二醛(MDA)、灌洗液蛋白浓度和细胞学变化;肺及血液SOD、GSH和Vit E。结果表明,大鼠在吸入H_2S后,MDA显著增加,灌洗液蛋白浓度明显增加,细胞学变化提示炎症反应明显。SOD活性先抑制后增强,GSH和Vit E在中毒后显著降低。上述各项指标变化的严重程度与硫化氢的吸入浓度有关。浓度高,损伤重,变化早,恢复慢。H_2S中毒导致自由基形成和脂质过氧化的增强是H_2S所致肺损伤的机制之一,其损伤程度与剂量有关。

The role of free radicals in the precipitation of lung damage after hydrogen sulfide inhalation was investigated in rats, which were killed right after and in the 1st, 6th,12th, 24th, and 72nd hour after exposure to 100 and 220 ppm of hydrogen sulfide (H2S) for 3 hours respectively. Malondialdehyde(MDA) level in lung homogenate and in bronchoalveolar lavage fluid (BALF), protein content and the number of leucocytes and pulmonary alveolar macrophages (PAM) in BALF, superoxide dismutase(SOD),glutathione(GSH),and vitamin E(VE)level in lung tissue and blood were determined. It was found that H2S inhalation resulted in an increase of MDA level which occurred much earlier after exposure to 220 ppm than after exposure to 100 ppm. Protein content was increased in the 1st, 6th, and 12th hour after inhalation. The number of leucocytes and PAM were increased, which implies the existence of inflammatory response in the respiratory tract. SOD activity decreased in the early period after inhalation but significantly increased later. Both GSH and VE levels decreasedThese findings suggest that H2S inhalation induces an inflammatory response in the respiratory tract and an increase of free radical formation which in turn brings about exessive lipid peroxidation. It is concluded that free radical formation is a contributing factor of lung damages after H2S inhalation.