The purpose of the Core Lipid Laboratory (CLL) is to provide state of the art lipid analysis for the research projects. Discussion between a project investigator and the CLL Director will be held to decide which type of assay would be most suitable and the form in which the samples should be provided to the CLL. The CLL staff will carry out the analytical procedures and provide a written report containing the data as well as an interpretation of the results. Another function of the CLL is developmental. When new areas of investigation are instituted, the CLL will set up any new lipid procedures that will be required. This may involve selecting a procedure available from the literature or, if necessary, developing a new approach. In addition, the CLL will assist the research projects in designing experiments that require extensive lipid analysis. The procedures that will be offered on a routine basis include: 1) fatty acid compositional analysis by gas-lipid chromatography (GLC); 2) analysis of radioactive fatty acids by reverse phase high-performance liquid chromatography (HPLC); 3) chemical preparation of samples for fatty acid GLC and HPLC, including extraction of lipids from tissue or plasma samples, methylation, saponification, silylation, acetylation, and hydrogenation; 4) separation of phospholipids and neutral lipids by thin-layer chromatography (TLC); 5) phospholipid class separation by HPLC; 6) phospholipids molecular species determination by HLPC; 7) eicosanoid separations by HPLC; 8) chemical measurements of the phospholipid, cholesterol, triglyceride, and free fatty acid content; 9) lipid peroxidation, using the thiobarbituric acid reacting substances (TBARS) method for screening purposes, and where positive results are indicated, either ethane collection or lipid hydroperoxide (LOOH) determination by iodometric assay; 10) tocopherol assay by HPLC; and 11) identification of fatty acids and oxidation products by GLC combined with mass spectrometry (MS), negative ion chemical ionization (NICI-MS) to determine the molecular ion, and electron impact (EI-MS) to obtain further structural information.

National Institute of Health (NIH)
National Cancer Institute (NCI)
Research Program Projects (P01)
Project #
Application #
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
Khoo, Nicholas K H; Hebbar, Sachin; Zhao, Weiling et al. (2013) Differential activation of catalase expression and activity by PPAR agonists: implications for astrocyte protection in anti-glioma therapy. Redox Biol 1:70-9
Carr, Wanakee J; Oberley-Deegan, Rebecca E; Zhang, Yuping et al. (2011) Antioxidant proteins and reactive oxygen species are decreased in a murine epidermal side population with stem cell-like characteristics. Histochem Cell Biol 135:293-304
Du, J; Liu, J; Smith, B J et al. (2011) Role of Rac1-dependent NADPH oxidase in the growth of pancreatic cancer. Cancer Gene Ther 18:135-43
Sun, Wenqing G; Weydert, Christine J; Zhang, Yuping et al. (2010) Superoxide Enhances the Antitumor Combination of AdMnSOD Plus BCNU in Breast Cancer. Cancers (Basel) 2:68-87
Simons, Andrean L; Mattson, David M; Dornfeld, Ken et al. (2009) Glucose deprivation-induced metabolic oxidative stress and cancer therapy. J Cancer Res Ther 5 Suppl 1:S2-6
Aykin-Burns, NĂ¹khet; Ahmad, Iman M; Zhu, Yueming et al. (2009) Increased levels of superoxide and H2O2 mediate the differential susceptibility of cancer cells versus normal cells to glucose deprivation. Biochem J 418:29-37
Sun, Wenqing; Kalen, Amanda L; Smith, Brian J et al. (2009) Enhancing the antitumor activity of adriamycin and ionizing radiation. Cancer Res 69:4294-300
Du, Changbin; Gao, Zhen; Venkatesha, Venkatasubbaiah A et al. (2009) Mitochondrial ROS and radiation induced transformation in mouse embryonic fibroblasts. Cancer Biol Ther 8:1962-71
Jacobs, Kristi Muldoon; Pennington, J Daniel; Bisht, Kheem S et al. (2008) SIRT3 interacts with the daf-16 homolog FOXO3a in the mitochondria, as well as increases FOXO3a dependent gene expression. Int J Biol Sci 4:291-9
Weydert, Christine J; Zhang, Yuping; Sun, Wenqing et al. (2008) Increased oxidative stress created by adenoviral MnSOD or CuZnSOD plus BCNU (1,3-bis(2-chloroethyl)-1-nitrosourea) inhibits breast cancer cell growth. Free Radic Biol Med 44:856-67

Showing the most recent 10 out of 163 publications