The urinary excretion and serum levels of retinol (Ret) and tocopherol (Toc) of 33 female university students were measured and their relationship examined. Serum and urinary levels of the kidney function parameters examined were within the normal ranges for the Japanese. The serum levels of Ret and Toc were 642 ng/ml and 7.71 μg/ml, respectively, and the Ret level showed a positive correlation with the level of Toc (r=0.45, p<0.01). Urinary excretion concentrations over 24 h (24hU) of Ret and Toc were 635 pg/ml and 2.23 ng/ml and the total amounts of excretion were 539 ng/day and 1.91 μg/day, respectively. In urinary 2nd-spot excretion (2ndU), the concentrations were 755 pg/ml for Ret and 2.77 ng/ml for Toc and the total excretion amounts of Ret and Toc were 129 and 459 ng for the total volume of 2ndU, respectively. Serum levels of Ret and Toc were not correlated with urinary excretion in 24hU and 2ndU. The urinary excretion concentration of Ret or Toc was not statistically different between those in 24hU and 2ndU, respectively. Urinary concentration of Ret in 24hU correlated with the total amounts of Ret in 24hU, and with the urinary concentration of Ret in 2ndU (r=0.56 and r=0.57, p<0.001, respectively). Also, 24 h urinary concentration for Toc was correlated with the total amounts of Toc in 24hU, and with the urinary concentration of Toc in 2ndU (r=0.41, p<0.05 and r=0.68, p<0.001, respectively). Urinary Ret concentration of 24hU or 2ndU was correlated with the concentration of Toc excretion in the 24 h or 2nd-spot urine (r=0.52, p<0.01 and r=0.57, p<0.001, respectively). Urine excretion concentrations of Ret and Toc showed a positive correlation with the levels of urinary creatinine (r=0.73 and r=0.75, p<0.001, respectively) and urea nitrogen (r=0.53 and r=0.46, p<0.01, respectively) of the kidney function index. This study shows that the urinary excretion of Ret and Toc was independent of their serum status, and that the urinary excretion concentration and total amounts of Ret and Toc of 24hU can be estimated from those of 2ndU.
Apoptosis and subsequent phagocytosis are two essential components of the surveillance process that is responsible for removing unwanted or damaged cells without inflammation. During phagocytosis, the exposure of phosphatidylserine (PS) on the cell surface is known to serve as a recognizable ligand (an “eat-me” signal) for macrophage receptors. A growing body of evidence suggests that reactive oxygen species (ROS) are generated during apoptosis triggered by a variety of stimuli and are involved in the initiation and execution of apoptosis. Recent studies have focused on a potential role of ROS and subsequent oxidative stress in signal transduction rather than being a trivial trigger of cell damage and apoptosis. A new concept has been proposed in which it is hypothesized that the selective oxidation of PS during execution of the (intrinsic) apoptotic program may serve as an important signal for the externalization of PS, which may then participate in fine-tuning of clearance of apoptotic cells by phagocytes. This hypothesis is discussed in the present review, along with, the molecular mechanisms underlying preferential PS oxidation and its association with redox catalysis by the cytochrome c released from mitochondria into the cytosol.
Oxidized low-density lipoprotein (OxLDL) is thought to be involved in the early development of atherosclerosis through foam cell formation. However, the actual nature of OxLDL found in vivo remained obscure until recently. We have established a sensitive method of measuring OxLDL present in human plasma by utilizing an anti-OxLDL monoclonal antibody, DLH3, together with an anti-apoB antibody. OxLDL levels appeared to increase in patients with acute myocardial infarction, cerebral infarction and several other pathological conditions. Evidence is accumulating which supports the close relation between vascular diseases and plasma OxLDL levels. In this article, a major concern is the source of the OxLDL. Our recent studies on the OxLDL present in both atherosclerotic lesions and in plasma, together with observations of minimally modified LDL, provide some further clues to the understanding of some of the features and behavior of OxLDL in the circulation. A possible scenario detailing the origin and dynamics of OxLDL in vivo is discussed.
Oxidative modification of low-density lipoprotein (LDL) is known to be a critical factor for pathogenesis of atherosclerosis. Several newly generated lipid components in the oxidatively modified LDL (oxLDL) have been shown to exert undesirable effects on various vascular cells. In particular, phosphatidylcholine (PC) having an oxidatively shortened fatty acyl group with a methyl, hydroxyl, oxo or carboxyl terminal attained interest, since they mimic diverse effects of platelet-activating factor (PAF), a mediator of inflammation, owing to their structural analogy to PAF. In this article, generation of PAF-like lipids in response to elevated oxidative stress due to cigarette smoking is documented, and its possible significance on atherogenesis is discussed.