Plant sterol oxidation products--analogs to cholesterol oxidation products from plant origin?

Cholesterol and plant sterols are lipids which are abundantly present in a western type diet of animal and plant origin, respectively. The daily intake averages 300 mg/day each. Over the past decades, a steadily increasing consumption of plant sterol enriched dairy products (2-3 g/day) took place to lower circulating LDL cholesterol concentrations. Like all unsaturated components, plant sterols can be attacked by reactive oxygen species resulting in plant sterol oxidation products (POPs). The most widespread methods for POP determination are high-performance liquid chromatography and gas-liquid chromatography. Yet, based on the low plasma POP concentrations in normophytosterolemic subjects (POPs: ∼0.3-4.5 ng/mL), a reliable quantification yielding an appropriate limit of detection remains a challenge. While the more abundantly present cholesterol oxidation products (COPs) have elaborately been studied, research on the metabolism and biological effects of POPs is only emerging. In relation to atherogenity, biological effects including modulation of cholesterol homeostasis, membrane functioning, and inflammation are attributed to POPs. Although mostly supra-physiological concentrations are applied in in vitro assays, anti-tumor activity, cytotoxicity and estrogen-competition have been attributed to specific POPs. However, it is not obvious, if and how POPs may exert in vivo adverse or beneficial health effects similar to those attributed to COPs. In the field of nutritional science, standardized methods for the determination of POPs are required to perform relevant biological studies and to assess their presence in complex foods or biological tissues and fluids. The aim of this review is to provide an overview and evaluation of the published methods and an update on the biological effects attributed to POPs.

[3H]Dopamine release by d-amphetamine from striatal synaptosomes of reserpinized rats.

The injection of reserpine, 5 mg/kg i.p. (ipRes), the regimen employed by a majority of investigators, results in synaptosomal and vesicular preparations which are incompletely reserpinized as determined by [3H]dopamine ([3H]DA) accumulation. Reserpine administered by the subcutaneous route, 5 mg/kg (scRes), appears to produce complete reserpinization. Release of [3H]DA by d-amphetamine (Amph) was observed from striatal synaptosomes prepared both from normal rats and those pretreated with reserpine intraperitoneally but not from those injected subcutaneously. In the more completely reserpinized scRes synaptosomes, so little [3H]DA had accumulated that release by Amph was not measurable, indicating that if a labile, reserpine-resistant, extravesicular DA storage pool releasable by Amph is present under these conditions, it must be extremely small. In scRes monoamine oxidase (MAO)-inhibited preparations, Amph released preloaded [3H]DA located in the cytosol in the absence of functional vesicles. Although chromatographic analysis of the superfusate from ipRes striatal synaptosomes showed that significant amounts of preloaded [3H]DA were released by Amph, the level of dihydroxyphenylacetic acid was not increased over controls, indicating that Amph releases only DA and not its metabolite and is also acting as a MAO inhibitor. No [3H]DA could be released by Amph from superfused hyposmotically shocked normal or ipRes synaptosomes, suggesting that an intact membrane is required for Amph-induced release.