Effects of physical stress on peroxide scavengers in normal and sickle cell trait erythrocytes☆

Das, Salil K.; Hinds, Joseph E.; Hardy, Robert E.; Collins, Jerry C.; Mukherjee, Sanjoy

doi:10.1016/0891-5849(93)90004-e

Cited by 29 publications

(21 citation statements)

References 36 publications

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“…However, since TNF-␣ remained unchanged and constitutes the major promoter of VCAM-1 expression on endothelial cells (29), it is possible that alternative pathways leading to activation of adhesion molecules may occur in response to initiation of alternative, hitherto unidentified, pathways. Among the potential explanations for such observations, catecholamines (6,33), other inflammatory molecules (5), and oxidative stress (12) could also underlie the excess induction of adhesion molecule concentrations as measured several hours after an acute maximal incremental exercise bout. Das et al (12) suggested that exposure of SCT subjects to treadmill exercise resulted in an increase of RBC oxidation associated with relatively excessive production of reactive oxygen species.…”

Section: Discussionmentioning

confidence: 99%

“…Among the potential explanations for such observations, catecholamines (6,33), other inflammatory molecules (5), and oxidative stress (12) could also underlie the excess induction of adhesion molecule concentrations as measured several hours after an acute maximal incremental exercise bout. Das et al (12) suggested that exposure of SCT subjects to treadmill exercise resulted in an increase of RBC oxidation associated with relatively excessive production of reactive oxygen species. The latter likely plays a role in triggering dysfunctional endothelium, which inactivates nitric oxide production, a vasodilator, and the expression of adhesion molecules within the endothelium (28,40).…”

Section: Discussionmentioning

confidence: 99%

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Effects of progressive and maximal exercise on plasma levels of adhesion molecules in athletes with sickle cell trait with or without α-thalassemia

Monchanin¹,

Serpero²,

Connes³

et al. 2007

Journal of Applied Physiology

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The aim of the study was to examine the effects of exercise on soluble vascular cell adhesion molecule-1 (sVCAM-1) and intercellular adhesion molecule-1 (sICAM-1) in sickle cell trait (SCT) athletes with or without α-thalassemia. Six athletes with SCT, seven athletes with both SCT and α-thalassemia (SCTAT), and seven control athletes (Cont) performed an incremental and maximal test on cycloergometer. Levels of sICAM-1 and sVCAM-1 were assessed at rest, immediately after the end of exercise, and 1, 2, and 24 h after exercise. Although Cont and SCTAT groups exhibited similar basal plasma levels of inflammatory and adhesion molecules, the SCT group had higher sVCAM-1 basal concentrations. Incremental exercise resulted in a significant increase of sVCAM-1 in all subjects, which remained elevated only in the SCT group during the recovery period. In conclusion, as sVCAM-1 increased with exercise and during the recovery period, our findings support the concept that SCT athletes might be at risk for microcirculatory disturbances and adhesive phenomena developing at rest and several hours after exercise. α-Thalassemia might be considered protective among exercising SCT subjects.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effects of progressive and maximal exercise on plasma levels of adhesion molecules in athletes with sickle cell trait with or without α-thalassemia

Monchanin¹,

Serpero²,

Connes³

et al. 2007

Journal of Applied Physiology

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“…To validate this activity, a SOD assay was performed using cytochrome c as described previously (Mukherjee et al, 1994;Das et al, 1993).…”

Section: Measurements Of Antioxidant Enzyme Activitymentioning

confidence: 99%

Benzo(a)pyrene‐induced acute neurotoxicity in the F‐344 rat: role of oxidative stress

Saunders

Das

Ramesh

et al. 2006

J of Applied Toxicology

152

125

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Given the link between neurotoxicity and exposure to pollutants, the potential behavioral neurotoxicity of benzo(a)pyrene [B(a)P] was investigated. Studies have established that B(a)P requires metabolic activation to highly reactive species to elicit many of its adverse effects. This study investigated the perturbation of nervous system function by correlating behavioral changes with the metabolism of B(a)P, antioxidant enzyme levels and lipid peroxidation in selected brain regions. The neurobehavioral effects of single oral doses of B(a)P (25-200 mg kg(-1) body weight) on motor activity were examined in male F-344 rats at 2, 4, 6, 12, 24, 48, 72 and 96 h post treatment. Parent B(a)P and metabolites were measured at the above mentioned time points by reverse phase HPLC. The activity of several antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) and levels of malondialdehyde were determined at 6 and 96 h in both the striatum and hippocampus of B(a)P exposed rats. Suppression of motor activity (up to 70%) reached a maximum at 6 h, but was reversible at 96 h in all dose groups. The kinetics of disposition data show a strong link between B(a)P metabolism and the onset and duration of behavioral effects. Benzo(a)pyrene caused a 15-70% inhibition in the activity of superoxide dismutase and glutathione peroxidase and an enhancement in catalase and lipid peroxidation (up to 68%) in the striatum and hippocampus at 6 and 96 h post treatment, respectively. These findings suggest that B(a)P-induced acute neurobehavioral toxicity may occur through oxidative stress due to inhibition of the brain antioxidant scavenging system.

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“…Patients with SCD also frequently report the development of vaso-occlusive symptoms after emotional and psychological stresses, changes in temperature, and physical exertion. [4][5][6] The molecular mechanism(s) by which these forms of stress may predispose to painful vaso-occlusive episodes has remained largely unexplored.Catecholamines released during stress stimulate adrenergic receptors (ARs), including the ␤-AR. These receptors, archetypal members of the G protein-coupled receptor superfamily, are expressed by RBCs 7 as well as by a variety of tissues throughout the body.…”

mentioning

confidence: 99%

Epinephrine-induced activation of LW-mediated sickle cell adhesion and vaso-occlusion in vivo

Zennadi¹,

Moeller²,

Whalen

et al. 2007

Blood

107

133

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Sickle red cell (SS RBC) adhesion is believed to contribute to the process of vaso-occlusion in sickle cell disease (SCD). We previously found that the LW RBC adhesion receptor can be activated by epinephrine to mediate SS RBC adhesion to endothelial alphavbeta3 integrin. To determine the contribution of LW activation to vaso-occlusive events in vivo, we investigated whether in vitro treatment of SS RBCs by epinephrine resulted in vaso-occlusion in intact microvasculature after RBC infusion into nude mice. Epinephrine enhanced human SS but not normal RBC adhesion to murine endothelial cells in vitro and to endothelium in vivo, promoting vaso-occlusion and RBC organ sequestration. Murine sickle RBCs also responded to epinephrine with increased adhesion to postcapillary endothelium in nude mice. Epinephrine-induced SS RBC adhesion, vaso-occlusion, and RBC organ trapping could be prevented by the beta-adrenergic receptor (beta-AR) antagonist, propranolol. Infusion of soluble recombinant LW also significantly reduced adhesion and vaso-occlusion. In addition, epinephrine-treated SS RBCs induced activation of murine leukocyte adhesion to endothelium as well. We conclude that LW activation by epinephrine via beta-AR stimulation can promote both SS RBC and leukocyte adhesion as well as vaso-occlusion, suggesting that both epinephrine and LW play potentially pathophysiological roles in SCD.

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Effects of physical stress on peroxide scavengers in normal and sickle cell trait erythrocytes☆

Cited by 29 publications

References 36 publications

Effects of progressive and maximal exercise on plasma levels of adhesion molecules in athletes with sickle cell trait with or without α-thalassemia

Effects of progressive and maximal exercise on plasma levels of adhesion molecules in athletes with sickle cell trait with or without α-thalassemia

Benzo(a)pyrene‐induced acute neurotoxicity in the F‐344 rat: role of oxidative stress

Epinephrine-induced activation of LW-mediated sickle cell adhesion and vaso-occlusion in vivo

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