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Biomedical subjects

C Deby

Publications and source records attributed to C Deby.

137 records · Page 8Linked to original sources
PubMedDate not supplied

Blood levels of reduced/oxidized glutathione and plasma concentration of ascorbic acid during eccentric and concentric exercises of similar energy cost.

In an attempt to assess the possible oxidative stress associated with the transient exercise-induced activation of polymorphonuclear neutrophils (PMN), we compared the effects of eccentric and concentric exercises (downhill run: DR and uphill walk: UW, respectively) of equal duration (35 min) and similar energy cost (60% VO2max) on plasma levels of ascorbic acid ([AA]) and blood concentration of reduced ([GSH]) and oxidized ([GSSG]) glutathione. Eight healthy male subjects took part in this study. Plasma concentration of myeloperoxidase ([MPO]) was used as a specific marker of PMN activation. While there were no significant changes in [MPO] and [AA] in UW experiments, [MPO] increased (+80%) and [AA] decreased significantly during DR tests (P < 0.01 and P < 0.05, respectively). A significant negative relationship was observed between [AA] and [MPO] in DR experiments only (r = -0.49; P < 0.01). Mean (+/- SEM) basal GSH and GSSG concentrations, calculated by pooling the values measured before both tests, were 0.54 +/- 0.02 and 0.12 +/- 0.007 mM, respectively. The blood concentration of these compounds remained practically unchanged in both exercise tests. These results confirm the role played by the eccentric component of muscle contraction in transient exercise-induced PMN activation and suggest that this activation was partly involved in the decrease in [AA] observed in DR experiments. The oxidant stress associated with the exercise protocol used in this study was insufficient to alter blood levels of reduced and oxidized glutathione.

Adult↗
PubMedDate not supplied

[Oxygen metabolism and toxicity in the phenomenon of ischemia-reperfusion].

One of the major cause of human disease results from the compromise of blood flow and oxygen delivery to tissues. Ischemia phenomenon is defined as blood flow that is inadequate to maintain normal tissue function. Prolonged ischemia ultimately results in irreversible changes in cell metabolism and cell death. Historically, it was felt that if ischemia results in altered cell function and injury, then reoxygenation or reperfusion leading to a restoration of a normal blood flow was expected to have a beneficial effect and promote salvage of tissue depending on the extent of ischemia. Recent studies have, however, revealed that reoxygenation leads to an oxygen metabolism resulting in the generation of active and toxic oxygen intermediates (free radicals) which play an important role in the pathophysiology of reperfusion injury.

Antioxidants↗
PubMedDate not supplied

Biochemical pathways of acute lung injury.

Complement fragments (C3, C3d, C5a), thromboxane B2 (TxB2), 6-keto-PGF1 alpha and immunoreactive trypsin (IRT) were measured in 98 patients at risk of developing the adult respiratory distress syndrome (ARDS): 53 multiple trauma, 28 abdominal surgery and 17 acute pancreatitis. Sixty-five of these patients developed ARDS: 30 multiple trauma, 19 abdominal surgery and 16 acute pancreatitis patients. Forty of the 65 ARDS patients and 9 out of the 33 non-ARDS patients died. Mean value of the C3d to C3 ratio was abnormal in both ARDS and non-ARDS patients. C5a-like activity was detected in 70 out of the 98 patients (49 ARDS and 22 non-ARDS patients). TxB2 abnormal values (greater than 100 pg . ml-1) were found in 70% of the patients, especially when sepsis occurred. No correlation could be made between abnormal 6-keto PGF1 alpha values and ARDS or sepsis. The mean peak IRT value was 675 micrograms . 1(-1) for ARDS patients and 274 micrograms . 1(-1) for non-ARDS patients (p less than 0.05). A firm correlation was also measured between IRT and sepsis (p less than 0.01). C5a-like activity was regularly detected soon after injury, while TxB2 and IRT tend to appear later in patients developing ARDS. Neither C3d/C3, nor C5a-like activity, nor TxB2, nor IRT are specific markers of ARDS, since they also appeared in severely ill patients who did not develop ARDS.

6-Ketoprostaglandin F1 alpha↗