Cigarette smoke-induced oxidative stress in skeletal muscles of mice.

Cigarette smoke (CS)-induced oxidative stress may cause muscle alterations in chronic conditions such as chronic obstructive pulmonary disease (COPD). We sought to explore in AKR/J mice exposed to CS for 6 months and in control animals, levels of protein oxidation, oxidized proteins (immunoblotting, proteomics) and antioxidant mechanisms in both respiratory and limb muscles, body weight modifications, systemic inflammation, and lung structure. Compared to control mice, CS-exposed animals exhibited a reduction in body weight gain at 3 months and thereafter, showed lung emphysema, and exhibited increased oxidative stress levels in their diaphragms and gastrocnemius at 6 months. Proteins involved in glycolysis, ATP production and distribution, carbon dioxide hydration, and muscle contraction were carbonylated in respiratory and limb muscles. Blood tumor necrosis factor (TNF)-alpha levels were significantly greater in CS-exposed mice than in control animals. In AKR/J mice, chronic exposure to CS induces lung emphysema concomitantly with greater oxidative modifications on muscle proteins in both respiratory and limb muscles, and systemic inflammation.

[Liver growth factor improves pulmonary fibrosis secondary to cadmium administration in rats]. / El factor de crecimiento de hígado mejora la fibrosis pulmonar inducida tras la administración de cadmio en ratas.

INTRODUCTION: Liver growth factor (LGF) is a liver mitogen with regenerating and anti-fibrotic activity even at extrahepatic sites. We used LGF in a lung fibrosis model induced by cadmium chloride (CdCl(2)), to study its antifibrotic capacity. METHODS: Forty-two male Wistar rats were administered a single dose of 0.5ml/rat of CdCl2 0.025% (n=21) or the same volume of saline (control group, n=21). After 35 days, once a lesion was established, we started a 3 week treatment with LGF, after which we determined lung function--inspiratory capacity (IC), lung compliance (LC), forced vital capacity (FVC) and expiratory flow at 75% (FEF75%)-, lung morphometry--alveolar internal area (AIA), mean linear intersection (LM)-, and collagen (both by Sirius red and hydroxyproline residues) and elastin contents. RESULTS: Pulmonary fibrosis in CdCl(2) rats was characterized by a marked decrease in pulmonary function with respect to healthy controls -reductions of 28% in IC, 38% in CL, 31% in FVC, and 54% in FEF75%- which was partially recovered after LGF injection -18% IC, 27% CL, 19% FVC and 35% FEF75%-; increase in collagen and elastin contents -165% and 76%, respectively, in CdCl2 rats, versus 110% and 34% after LGF injection-; and increases in AIA and LM, partially reverted by LGF. CONCLUSIONS: Together, these data seem to demonstrate that LGF is able to improve lung function and partially reverts the increase in lung matrix proteins produced by CdCl(2) instillation.