Stigmasterol dealkylation

Insects, unlike most vertebrates and plants, lack the capacity for de novo sterol synthesis and require dietary sterol for their normal growth, development and reproduction. This sterol requirement is in most cases satisfied by cholesterol (86) which is one of the principal sterols in insects, serving as component of the cell membranes and as a precursor of ecdysone (107). The zoophagous species such as the house fly Mucosa domestica are unable to convert phytosterol to cholesterol. For this reason, cholesterol is an essential nutrient for these species. In phytophagous and omnivorous insects, sterols such as sitosterol (87), campesterol (88), and stigmasterol (89) are dealkylated to cholesterol. Thus, 24-dealkylation is one of the essential metabohc processes in phytophagous insects (Fig. 15). 

In the case of stigmasterol (89), the proposed mechanism in Fig. 18 was evaluated as follows. [23- H]-, [24- H]- and [25- H]stigmasterols were synthesized and the fate of the deuterium atoms during the dealkylation was followed by mass spectrometry. The transfer of the deuterium atom from C-25 to C-24 was established in silkworm larvae [162]. Also, the chemically synthesized (24F)- and (24Z)-A -dienes (93 and 94) were found to satisfy the sterol requirement of the silkworm. The A -diene (96) and desmosterol (91) were identified in significant amounts from the insects in accord with the previous observation by the Beltsville group. However, mass fragmentographic analysis of the sterols of insects fed on stigmasterol (89), the... 

In stigmasterol-supplemented cultures (Table III), N.N-dimethyldodecanamine caused the accumulation of a number of and A 2,24 sterols, including the 22,24 analogue of fucosterol stigmasta-5,22E,24(28)-trienol. Presence of this compound and lack of detection of fucosterol and 5,22, a5,7,22 or A7,22 dealkylated sterols... 

As mentioned earlier, much of the information on dealkylation and conversion of C28 and C29 phytosterols to cholesterol in insects (Figure 2) has been acquired through research with two lepidopteran species, the tobacco homworm, Af. sexta (3, and references therein) and the silkworm, B. mori (5, and references therein). Studies with Af. sexta established that desmosterol is the terminal intermediate in the conversion of all phytosterols to cholesterol, and that fucosterol and 24-methylenecholesterol were the first intermediates in the metabolism of sitosterol and campesterol, respectively, to cholesterol (5). In-depth metabolic studies with B. mori first demonstrated the involvement of an epoxidation of the A - -bond of fucosterol or 24-methylenecholesterol in the dealkylation of sitosterol and campesterol (5,45). More recently, the metabolism of stigmasterol was elucidated in detail in another lepidopteran, Spodoptera littoralis, and the side chain was shown to be dealkylated via a A " -bond and a 24,28-epoxide as were sitosterol and campesterol (46). The only significant differences in the metabolism of stigmasterol are the involvement of the additional 5,22,24-triene intermediate preceding desmosterol in the pathway and reduction of the A -bond prior to reduction of the A -bond (Figure 2). 

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