Levels of oxidative stress were assessed by measuring malondialdehyde and protein carbonylation.
2
The concentration of malondialdehyde in serum did not change with the estrogen-progestin treatment.
3
Lipid peroxidation recorded an increase revealed by high femur malondialdehyde levels.
4
The antiaggregating activity and the inhibition of platelet malondialdehyde production were studied in vitro.
5
In addition, plasma total and free L-carnitine concentrations were negatively correlated with malondialdehyde levels.
6
Histopathology and malondialdehyde assay were performed on pancreatic tissue samples.
7
Taurine deficiency also predisposed the heart to enhanced formation of malondialdehyde caused by doxorubicin administration.
8
The content of malondialdehyde in aortic tissue did not change after oxidative stress or alpha-tocopherol pretreatment.
9
Quercetin also increased serum albumin and hepatic glutathione levels and reduced the hepatic level of malondialdehyde.
10
Serum inflammatory markers of muscle damage, including malondialdehyde.
11
Proanthocyanidins also restored serum albumin and total protein levels, and reduced the hepatic level of malondialdehyde.
12
Results: No significant difference was observed in lung tissue nitrite and malondialdehyde levels among the study groups.
13
Levels of lipid peroxidation product malondialdehyde have been recently correlated with clinical grades of oral Submucous fibrosis.
14
During enzyme replacement therapy, there was a significant reduction in levels of malondialdehyde when compared to pretreatment.
15
Reoxygenation was without any effect on catalase activity, but a significant increase in the malondialdehyde content was seen.
16
The protective effect of alpha-tocopherol was related to significantly decreased malondialdehyde and significantly increased tissue concentrations of alpha-tocopherol.