| First Author | Schock BC | Year | 2004 |
| Journal | Arch Biochem Biophys | Volume | 423 |
| Issue | 1 | Pages | 162-9 |
| PubMed ID | 14871478 | Mgi Jnum | J:146717 |
| Mgi Id | MGI:3838283 | Doi | 10.1016/j.abb.2003.12.009 |
| Citation | Schock BC, et al. (2004) Enhanced inflammatory responses in alpha-tocopherol transfer protein null mice. Arch Biochem Biophys 423(1):162-9 |
| abstractText | The liver preferentially secretes alpha-tocopherol into plasma under the control of the hepatic alpha-tocopherol transfer protein (alpha-TTP). alpha-TTP-null mice (Ttpa(-/-) mice) are vitamin E deficient, therefore were used for investigations of in vivo responses to sub-normal tissue alpha-tocopherol concentrations during inflammation. Increased basal oxidative stress in Ttpa(-/-) mice was documented by increased plasma lipid peroxidation, and superoxide production by bone marrow-derived neutrophils stimulated in vitro with phorbol 12-myristate 13-acetate. Lipopolysaccharide (LPS) injected intraperitoneally induced increases in lung and liver HO-1 and iNOS, as well as plasma NO(x) in Ttpa(+/+) mice. LPS induced more modest increases in these markers in Ttpa(-/-) mice, while more marked increases in plasma IL-10 and lung lavage TNF alpha were observed. Taken together, these results demonstrate that alpha-tocopherol is important for proper modulation of inflammatory responses and that sub-optimal alpha-tocopherol concentrations may derange inflammatory-immune responses. |
