Oxidative Stress and Nitric Oxide in Sedentary Older Adults with Intellectual and Developmental Disabilities.

Individuals with moderate-to-profound intellectual and developmental disabilities (IDD) are characterized by significant cognitive deficits, abnormal muscle tone, poor posture and balance, and inactive lifestyle. Increased oxidative stress (OS) has been implicated in a variety of chronic diseases, inflammatory conditions, aging, and even following intense physical exercise. Nitric oxide (NO) is a highly reactive mediator that has been shown to play different roles in a variety of different biological process and in aging. The aim of the study was to investigate the serum levels of global OS and NO metabolites (NOx) in sedentary and non-sedentary older adults with IDD. Global OS was measured by CR 3000 instrument, FORM system, and NOx were measured by determination of serum nitrite levels. OS and NOx levels were significantly higher in sedentary IDD comparing non-sedentary controls. The increased of OS and NOx levels suggest their possible involvement in the phenomenon of 'accelerated aging' in IDD. Our findings can provide another aspect indicating both OS and NOx as possible biochemical markers and their potential application in minimizing their negative influence through future therapeutic strategies.

Body composition in heavy smokers: comparison of segmental bioelectrical impedance analysis and dual-energy X-ray absorptiometry.

Smokers tend to have lower body mass index, on one hand, and increased abdominal obesity, on the other hand. Also, low levels of lean mass (LM) and bone mineral content (BMC) were found among older smokers compared with non-smokers. This altered body composition and its consequences raise the need for simple and reliable methods for assessment of body composition in smokers. This study aimed to compare body composition assessment by segmental bioelectrical impedance analysis (sBIA) with the reference method, dual energy X-ray absorptiometry (DEXA). Body composition was measured by sBIA (Tanita BC-545) and DEXA (Hologic) in 49 heavy smokers (>15 cigarettes/day, mean age 43.8±12.0). The comparison included correlations and differences between measurements obtained using the two methods as well as the Blande-Altman analysis. Whole-body fat mass (FM) and LM measured by the two methods were found to be highly correlated (r>0.9, p<0.001). Compared with DEXA, sBIA significantly overestimated whole-body LM and BMC (1,126 g and 382 g, respectively, p<0.01). The Bland-Altman analysis revealed a good agreement for whole-body FM and LM, but a poor agreement for BMC. The segmental FM percentage and LM were also highly correlated (r>0.9, p<0.001). However, sBIA significantly overestimated LM of the trunk and legs and underestimated the appendicular FM percentage. Verified by DEXA, sBIA provides reliable measures of whole-body LM, FM, and trunk FM in heavy smokers. A lesser degree of agreement was found for BMC, appendicular LM, and FM.

Peroxynitrite induces degradation of myosin heavy chain via p38 MAPK and muscle-specific E3 ubiquitin ligases in C2 skeletal myotubes.

Oxidative stress and inflammation play an important role in the catabolism of skeletal muscles. Recently, cigarette smoke (CS) was shown to stimulate muscle catabolism by activation of p38 MAPK and up-regulation of the muscle-specific E3 ubiquitin ligases (E3s) atrogin-1 and MuRF1 which are over-expressed during muscle atrophy. Peroxynitrite (ONOO-), an oxidative ingredient of CS, also produced during oxidative stress and inflammation, was previously shown to induce ubiquitination and degradation of muscle proteins. To investigate the involvement of p38 MAPK and the muscle-specific E3s in ONOO--induced muscle catabolism, C2 myotubes, differentiated from a myoblast cell line, were exposed to ONOO- (25 µM) in a time-dependent manner. Following exposure, degradation of myosin heavy chain (MyHC) and actin, activation of p38 MAPK, and levels of atrogin-1 and MuRF1 were studied by Western blotting. Peak phosphorylation of p38 MAPK was observed at 1 h of ONOO- exposure. ONOO- caused a significant increase in the levels of atrogin-1 and MuRF1. In accordance, a significant decrease in MyHC levels was observed in a time-dependent manner. These findings support previous studies in which the catabolic effects of ONOO- were shown. In addition, ONOO- was demonstrated to induce degradation of muscle proteins by activation of p38 MAPK and up-regulation of the muscle-specific E3s atrogin-1 and MuRF1.

Relationship between history of smoking, metabolic and inflammatory markers, parameters of body composition and muscle strength.

The objective of this study was to investigate the relationship between smoking history expressed by pack-years, metabolic and inflammatory markers, parameters of body composition (BC) and muscle strength among heavy smokers. A detailed smoking history was obtained from 49 heavy smokers (age = 44 ± 12, pack-years = 31 ± 23). Blood samples were analyzed for levels of glucose, lipids, liver enzymes and C-reactive protein (CRP). Anthropometric measurements included waist circumference and assessment of BC by dual energy X-ray absorptiometry (DEXA) and bioelectrical impedance analysis (BIA). Muscle strength was assessed by handgrip dynamometry and predicted one-repetition maximum (p1RM) tests. Positive correlations were found between pack-years of smoking, fasting glucose, alkaline phosphatase and CRP levels. Pack-years were also positively correlated with waist circumference, body mass index (BMI), whole-body and trunk fat mass measured by both DEXA and BIA. A negative correlation was found between pack-years of smoking and muscle strength measured by p1RM for the leg press exercise. After adjustment for age, sex and BMI, a positive correlation remained between pack-years of smoking and CRP levels. In conclusion, after controlling for possible confounders, smoking history was found to be positively associated with CRP levels among heavy smokers.