An isocratic HPLC method has been developed to determine riboflavin in eggs, whole milk, 2% fat milk, skim milk, dry milk, yogurt, cottage cheese, and cheddar cheese. T'he developed method involves acidification, centrifugation, and quantification of riboflavin in the supernatant with HPLC. The HPLC system consisted of a p Bondapak Cl8 column, a solvent system of water-methanol-acetic acid (68:32:0.1 v/v), a flow rate of 1.0 ml/min, and a UV detector. The method is simple, rapid, sensitive, and specific for riboflavin. Recoveries of more than 90% were obtained in all samples analyzed.

Raw beef, pork, veal, lamb, chicken, turkey, and duck have been identified with a liquid chromatographic (LC) method. Meat samples are blended in water, and soluble proteins in the aqueous blends are separated by the LC method. Meat cuts and parts from same species had similar chromatographic profiles and differed only quantitatively. However, meat cuts or parts from different species resulted in different chromatographic profiles. The qualitative and quantitative chromatographic differences among meat species were used for their identification. The LC method applies only to fresh and frozen meats. It is simple, rapid, and reliable, and can be used for quantitative detection of meat species in unheated meat blends.

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Recently, formaldehyde (FA), existing in a number of different cells including neural cells, was found to affect age-related cognitive impairment. Oral administration of methanol (the metabolic precursor of FA) triggers formation of senile plaques (SPs) and Tau hyperphosphorylation in the brains of monkeys with memory decline. Intraperitoneal injection of FA leads to hyperphosphorylation of Tau in wild-type mouse brains and N2a cells through activation of glycogen synthase kinase-3β (GSK-3β). Furthermore, formaldehyde at low concentrations can directly induce Tau aggregation and amyloid β (Aβ) peptide deposits in vitro. Formaldehyde-induced Tau aggregation is implicated in cytotoxicity and neural cell apoptosis. Clarifying how FA triggers Aβ deposits and Tau hyperphosphorlyation will not only improve our understanding of the molecular and cellular mechanisms of age-related cognitive impairment but will also contribute to the ongoing investigation of alternate targets for new drugs. Here, we review the role of FA, particularly that of endogenous origin, in protein aggregation and as a potential drug intervention in the development of agerelated cognitive impairment.