Catalase and glutathione peroxidase activity in cells with trisomy 21

Crosti, N.; Bajer, Jolanta; Gentile, Mariangela; Resta, G; Serra, Angelo

doi:10.1111/j.1399-0004.1989.tb03172.x

Cited by 25 publications

(5 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Indeed, increased activity of GPx in DS neutrophils is consistent with the results of previous studies [Kedziora and Bartosz, 1988;Muchová et al, 2001] and is most likely induced by increased H 2 O 2 production, a substrate for GPx [Rhee et al, 2005]. In agreement with other studies, no significant difference was observed in the activity of CAT and MPO, two other enzymes that catalyze the decomposition of H 2 O 2 [Kedziora and Bartosz, 1988;Crosti et al, 1989].…”

Section: Discussionsupporting

confidence: 94%

Neutrophil oxidative metabolism in Down syndrome patients with congenital heart defects

Akıncı

Mıhçı

Taçoy

et al. 2009

Environ and Mol Mutagen

View full text Add to dashboard Cite

Down syndrome (DS) occurs when an individual has three, rather than two, copies of the 21st chromosome. Cytosolic superoxide dismutase (SOD-1) is encoded by a gene on chromosome 21 and thus, SOD-1 activity is elevated in patients with DS. Forty percent of all cases with DS are associated with congenital heart defects (CHD). Although the contribution of SOD1 to disease phenotype is unknown, it is considered to be a "molecular marker" of the disease. It was hypothesized herein that the presence of CHD may alter the expression of SOD1 and oxidative metabolism in patients with DS. This hypothesis was tested via four experimental groups as follows: patients with DS without CHD, DS patients with CHD, CHD patients without DS and controls. Expression and activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), myeloperoxidase (MPO), and catalase (CAT) were determined in neutrophils from all experimental groups. Intracellular hydrogen peroxide concentration and superoxide release were also evaluated in neutrophils. A significant increase was observed in SOD and GPx amount and activity in patients with DS with and without CHD. No significant difference was found in the amount and activity of MPO and CAT among the different experimental groups. Intracellular hydrogen peroxide concentration was similar in all groups, whereas a prominent decrease was seen in superoxide release in cases with DS. Patients with DS with and without CHD showed no significant differences in any of the measured parameters. The data suggest that CHD observed in patients with DS does not result from altered redox metabolism associated with the disease.

show abstract

Section: Discussionsupporting

confidence: 94%

Neutrophil oxidative metabolism in Down syndrome patients with congenital heart defects

Akıncı

Mıhçı

Taçoy

et al. 2009

Environ and Mol Mutagen

View full text Add to dashboard Cite

show abstract

“…Consequently, it is likely that the activities of the antioxidant enzymes in the first and second steps are balanced to prevent oxidative damage. 6 SOD overexpression in people with Down's syndrome unbalances this equation, which may ultimately lead to increased H 2 O 2 production. This indicates that trisomic cells are more sensitive to oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Regular exercise did not modify significantly superoxide dismutase activity in adolescents with Down’s syndrome

Ordóñez

Rosety²,

Rosety-Rodriguez³

2006

Br J Sports Med

View full text Add to dashboard Cite

Regular exercise did not significantly increase SOD activity and consequently did not affect the unbalanced equilibrium SOD/glutathione peroxidase+catalase observed in patients with Down's syndrome. Further studies are required to assess the behaviour of other antioxidant enzymes included in this pathway in order to highlight potential benefits of regular exercise in redox metabolism of patients with Down's syndrome.

show abstract

“…These patients possess in their cells three instead of the usual two copies of the Cu/Zn superoxide dismutase (SOD) gene (Antila and Westermarck, 1989), located in the 21q21.2e21q22.3 segment (Korenberg, 1993;Gardiner et al, 2005). The imbalance between SOD and peroxidase, brought about by the increased activity of the Cu/Zn SOD-1 (Groner et al, 1986), is responsible for the high oxidative stress these patients display (Crosti et al, 1989). This is accompanied by increased endogenous DNA damage in interphase, and, through G2 checkpoint adaptation, by the subsequent appearance of chromosomal aberrations in the subsequent metaphase (Bernstein and Bernstein, 1991).…”

Section: Introductionmentioning

confidence: 99%

G2 checkpoint‐dependent DNA repair and its response to catalase in Down syndrome and control lymphocyte cultures

Pincheira

Romero

Marcelain

et al. 2007

Cell Biology International

View full text Add to dashboard Cite

The amount of DNA lesions repaired in G2 and also G2 timing are controlled by the DNA damage-dependent checkpoint. Down syndrome (DS) lymphocytes showed twice as much constitutive DNA damage in G2 than control ones, when recording it as chromosomal aberrations in metaphase, after caffeine-induced checkpoint abrogation. During G2, DS lymphocytes repaired 1.5 times more DNA lesions than control ones. However the DS cells displayed a decreased threshold for checkpoint adaptation, as the spontaneous override of the G2 to mitosis transition block induced by the checkpoint took place in the DS cells when they had three times more DNA lesions than controls. Catalase addition to cultures scavenges hydrogen peroxide diffused from cells, resulting in subsequent intracellular depletion (Antunes and Cadenas, 2000). The intracellular H2O2 level seemed to regulate the G2 checkpoint. Thus, in controls, H2O2 depletion (induced by 3.2-50 microg/mL catalase) prevented its functioning: chromosomal damage increased while G2 shortened. Conversely, in the DS lymphocytes, 12.5 microg/mL catalase lengthened G2 and decreased chromosomal damage, in spite that the amount of DNA repaired in G2 was half of that repaired in the catalase-free DS lymphocytes.

show abstract

Catalase and glutathione peroxidase activity in cells with trisomy 21

Cited by 25 publications

References 32 publications

Neutrophil oxidative metabolism in Down syndrome patients with congenital heart defects

Neutrophil oxidative metabolism in Down syndrome patients with congenital heart defects

Regular exercise did not modify significantly superoxide dismutase activity in adolescents with Down’s syndrome

G2 checkpoint‐dependent DNA repair and its response to catalase in Down syndrome and control lymphocyte cultures

Contact Info

Product

Resources

About