Effect of 2 ppm ozone exposure on rat lung lipid fatty acids

Based on in vitro studies, the initial damage to lung cells by ozone exposure is believed to result in part from the breakdown of lipid polyunsaturated fatty acids to aldehydes, ozonides, and peroxides. The present study measured lipid breakdown products in lungs isolated from rats pretreated with [1-14C]acetate 12 h before exposure for 4 h to either air or 2 ppm ozone. Lipid fatty acid breakdown was indicated by a 112% increase in thiobarbituric acid-reactive substances on ozone exposure and by changes in chemical and radioactive measurements of mono- and dicarboxylic acids formed by treatment of lipid fractions with hydrogen peroxide. Ozone exposure resulted in a 63% increase in recovery of short-chain fatty acids accounted for by increased recoveries of malonic acid by 37%, hexanoic acid by 47%, nonanoic acid by 118%, and azelaic acid by 107%. Recovery of glutaric acid was enhanced 15-fold by ozone exposure. Although decreases in tissue arachidonic acid could not be detected, oleic acid was significantly decreased by 36%. Recovery of radiolabel as short-chain fatty acids was increased by 65% on ozone exposure and was mainly accounted for by enhanced labeling of nonanoic and glutaric acid fractions. The failure to observe significant increases in 14C recovery in the other fractions suggested ozone-induced breakdown of unlabeled fatty acids. These results demonstrate the cleavage of unsaturated fatty acid double bonds following in vivo exposure of lungs to ozone. Breakdown of arachidonic and oleic acids was specifically identified by increased recoveries of glutaric and nonanoic acids, respectively.     

Shoulder instability: impact of glenohumeral arthrotomography on treatment

We used arthrotomography to study the glenoid labrum in 114 patients. Sixty-nine of the patients had anatomic instability of the shoulder (including recurrent dislocation and subluxation of the shoulder), and 45 patients had functional instability of the shoulder (denoted by chronic pain, clicking of the joint, and the sensation that an unstable condition exists without the objective signs of it). Labral tears were revealed arthrotomographically in 86% of the patients with anatomic instability, while only 40% of the patients with functional instability had labral abnormalities, and these were primarily of minor severity. Fifty-six patients (44 of whom had anatomic instability; 12, functional instability) required surgery. The surgical findings were correlated with the arthrotomographic findings, and no false-positive results were revealed. However, arthrotomography demonstrated only part of the pathologic condition of two patients. These results confirm that there is a strong correlation between labral pathologic conditions and anatomic instability of the shoulder. Arthrotomographic studies have a great impact on the selection of therapy in cases of both anatomic and functional instability of the shoulder.     

Adaptation of a perfused rat hemidiaphragm preparation to the study of intermediary metabolism

Glucose catabolism of a vascular perfused rat hemidiaphragm was determined at rest and during stimulation of the phrenic nerve with trains of either 5 (T5) or 15 (T15) pulses (20 msec intervals) per second. Tissues were perfused and bathed in HEPES-buffered medium containing 11 mM D-[U-14C, 5-3H]glucose, equilibrated with 100% O2. Resting glucose catabolism via the Emden-Meyerhof pathway was indicated by a 3H2O production rate per hemidiaphragm of 1.45 +/- 0.07 mumol/h, of which 47% was recovered as [14C]lactate with the remainder assumed to be metabolised by mitochondria. During the first 30 min of T5 and T15 stimulation, peak isometric tension declined from an initial value of 105 +/- 8 g by 54% and 79%, respectively. The resulting peak tensions of 48 and 22 g remained constant for the next 60 min. These tensions were associated with linear rates of 3H2O production of 2.93 +/- 0.41 and 2.84 +/- 0.25 mumol/h. Stimulation by T5 and T15 increased mitochondrial metabolism of glucose by 64% and 95%, respectively, with no significant alterations in lactate formation from either exogenous or endogenous sources. The results suggest that the initial decline in tension is due to fatigue of the fast anaerobic myofibers; whereas, the sustained force beyond 30 min is attributable to the mitochondrial-rich slow myofibers.     

Interferon-induced depressive illness in hep C patients responds to SSRI antidepressant treatments

This paper examines the role of selective serotonin reuptake inhibitors (SSRIs) in the treatment of hepatitis-C virus (HCV) patients who have developed interferon-α induced depression. A 2-year data analysis of HCV psychiatric liaison clinic has been undertaken. The diagnosis, treatment, and progress of those patients who were treated with interferon-α (INF-α) are reported. 53 of the 78 patients enrolled at the HCV Clinic and treated with INF-α were referred for psychiatric consultation. Six patients developed major depressive illness following INF therapy. They were all treated with SSRIs and they made full recovery. This is a significant observation and is concordant with other studies. Its biochemical ramifications are presented. It is concluded that INF-induced depression is fully reversible. A hypothesis is proposed that SSRIs modulate the neuro-protective neurotoxic ratio by possibly inhibiting the indole-2,3-dioxygenase induction of the kynurenine pathway.