Low-concentration ozone reacts with plasmalogen glycerophosphoethanolamine lipids in lung surfactant.

Ozone is a common environmental toxicant to which individuals are exposed to on a daily basis. While biochemical end points such as increased mortality, decrements in pulmonary function, and initiation of inflammatory processes are known, little is actually understood regarding the chemical mechanisms underlying changes in pulmonary health, especially for low concentrations of ozone. This study was undertaken to investigate ozone-induced oxidation of endogenous lipids that are potentially exposed to environmental ozone within lung, specifically focusing on plasmalogen glycerophospholipids present in pulmonary surfactant. Sensitive liquid chromatography-mass spectrometry methods were developed to follow oxidation of diacyl and plasmalogen phosphatidylethanolamine (PE) phospholipids and to identify and quantitate products generated by ozonolysis. Using a unilamellar vesicle system containing a 1:1 molar mixture of 1-O-octadec-1'-enyl-2-octadecenoyl-PE and 1,2-dihexadecanoyl-PC, these studies revealed that the vinyl ether bond of plasmalogens was oxidized preferentially at low concentrations of ozone (100 ppb), when compared to olefinic bond oxidation on omega-9 of the fatty acyl chain in the same phospholipids. Major phospholipid products generated were identified as 1-formyl-2-octadecenoyl-PE and 1-hydroxy-2-octadecenoyl-PE. Heptadecanal and heptadecanoic acid production was also quantitated using gas chromatography-mass spectrometry, and production was consistent with oxidation of the vinyl ether, at low concentrations of ozone. Analysis of murine lung surfactant from C57Bl/6 mice revealed several plasmalogen PE lipid species, encompassing approximately 38% of total PE species. Upon exposure of ozone (0 and 100 ppb) to murine surfactant, plasmalogen PE molecular species preferentially reacted, as compared to diacyl PE molecular species. Lysophospholipids, pentadecanal, and nonanal were found to be the primary products of surfactant ozone oxidation.

Long-Term Administration of Queen Bee Acid (QBA) to Rodents Reduces Anxiety-Like Behavior, Promotes Neuronal Health and Improves Body Composition.

BACKGROUND: Queen bee acid (QBA; 10-hydroxy-2-decenoic acid) is the predominant fatty acid in royal jelly (RJ) and has activity at estrogen receptors, which affect brain function and body composition. However, few, long-term studies have assessed QBA effects in brain health and body composition. METHODS: Primary hippocampal neurons were treated with QBA (0-30 µM) and challenged with glutamate or hypoxia. QBA was fed to aged, male Sprague-Dawley rats (12-24 mg/kg/day) and to adult male and female Balb/C mice (30-60 mg/kg/day) for ≥3.5 months. Rats were evaluated in a behavioral test battery of brain function. Mice were measured for fat and muscle composition, as well as bone density. RESULTS: QBA increased neuron growth and protected against glutamate challenge and hypoxia challenge. Rats receiving QBA had reduced anxiety-like behavior, increased body weight, and better maintenance of body weight with age. Mice receiving QBA exhibited increased body weight, muscle mass, and adiposity in males, and increased bone density, but decreased adiposity, in females. CONCLUSIONS: QBA is an active component of RJ that promotes the growth and protection of neurons, reduces anxiety-like phenotypes, and benefits bone, muscle and adipose tissues in a sex-dependent manner, which further implicates estrogen receptors in the effects of QBA.