In homogenous solution, cholesterol autoxidation leads to am ixture of epimers of 5 primary products,whose concentrations vary in the presence/absence of antioxidants,such as vitamin E. Tw oo ft he products (5a-OOH and 6b-OOH) undergo Hockf ragmentation to yield electrophilic secosterols implicated in disease.H erein, we show that the product distribution is similar in phospholipid bilayers,i nt hat the 7-OOHs are the major products,but the presence/absence of vitamin Ehas no effect on the distribution. Cholesterol 7a-OOH, but not 7b-OOH, undergoes Hockfragmentation to yield am ixture of unprecedented A-ring cleavage products and 6,7-epoxides.W hen subjected to typical derivatization conditions,7 a-OOH yields products with essentially indistinguishable chromatographic and spectroscopic features from the previously identified secosterols,c asting further doubt on their controversial origin from endogenous O 3 .

In homogenous solution, cholesterol autoxidation leads to a mixture of epimers of 5 primary products, whose concentrations vary in the presence/absence of antioxidants, such as vitamin E. Two of the products (5α‐OOH and 6β‐OOH) undergo Hock fragmentation to yield electrophilic secosterols implicated in disease. Herein, we show that the product distribution is similar in phospholipid bilayers, in that the 7‐OOHs are the major products, but the presence/absence of vitamin E has no effect on the distribution. Cholesterol 7α‐OOH, but not 7β‐OOH, undergoes Hock fragmentation to yield a mixture of unprecedented A‐ring cleavage products and 6,7‐epoxides. When subjected to typical derivatization conditions, 7α‐OOH yields products with essentially indistinguishable chromatographic and spectroscopic features from the previously identified secosterols, casting further doubt on their controversial origin from endogenous O3.

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