Direct inhibition of (Z)-9 desaturation of (E)-11-tetradecenoic acid by methylenehexadecenoic acids in the biosynthesis of Spodoptera littoralis sex pheromone.

G Fabrias,L Gosalbo,J Quintana,F Camps

doi:10.1016/s0022-2275(20)39134-3

Abstract

Analysis by gas chromatography coupled to mass spectrometry demonstrated that 11,12-methylenehexadec-11-enoic acid and 12,13-methylenehexadec-12-enoic acid are beta-oxidized in Spodoptera littoralis sex pheromone gland to 9, 10-methylenetetradec-10-enoic acid and 10,11-methylenetetradec-10-enoic acid, respectively. This result supported our previous hypothesis that inhibition of the (Z)-9 desaturation of (E)-11-tetradecenoic acid by those C-16 fatty acids is actually caused by their corresponding beta-oxidation products. However, although (2,2,3,3-2H4)-11,12-methylenehexadec-11-enoic acid was not chain-shortened to the C-14 derivative, its activity as inhibitor of the (Z)-9 desaturation reaction was similar to that exhibited by 11,12-methylenehexadec-11-enoic acid. Therefore, the C-16 cyclopropene fatty acids may inhibit the (Z)-9 desaturation enzyme by themselves, probably through interaction of the cyclopropene ring with a binding site of the enzyme with the substrate double bond.

Highlights

Evidence that two naturally occurring cyclopropene fatty acids (CPFA) inhibited the desaturation of stearic to oleic acid was first presented in vertebrate systems by Reiser and Raju [1].These compounds, named sterculic and malvalic acids, have 18and 17carbon atoms, respectively, with the cyclopropene ring at positions 9,lO and 8,9.It was later shown that both acids inhibited the 9,lO-desaturation of different C-12 to C-20 aliphatic acids, regardless of the chain length [2].The importance of the ring position upon the effectiveness of the 9,lO-desaturation inhibition was studied by Fogerty,Johnson and Pearson [3],who found that only when the ring was included in the C-9 and/or
In agreement with this assumption, synthetic 10,ll-methylenetetradec-1Oenoicacid (10MTA), resulting from a putative P-oxidation of 12-(2-16 cyclopropene fatty acid or methylenehexadecenoic acid (MHA) in the gland, inhibited the above (Z)-9 desaturation reaction [8].In this article we demonstrate that P-oxidation of the above mentioned MHAs does occur in the pheromone gland
The first objective of this work was to experimentally prove that chain-shortening of MHAs to the corresponding C-14 cyclopropene fatty acid or methylenetetradecenoic acid (MTA) occurred in the pheromone gland

Summary

Introduction

On the basis of Fogerty et al [3]structure-activity relationship studies, the latter effect of the above 11,12-methylenehexadec-ll-enoiaccid (11-MHA) and 12,13-methylenehexadec-12-enoiaccid (12-MHA) was unexpected, as they did not fulfill one of the critical structural requirements to inhibit the (Z)-9 desaturase enzyme, namely neither C-9 nor C-10, which are the positions desaturated in El 1- 14:Acid,were included in the cyclopropene ring This requirement would be present in the corresponding C-14 cyclopropene fatty acids (MTAs, see Fig. 1)that would arise from chain-shortening of those MHAs. we suggested that both 11-MHAand 12-MHAcould be Poxidized in the insect pheromone gland to give the corresponding MTAs, which would be the real active compounds on the (Z)-9 desaturase enzyme. We present additional evidence that both 11-MHAand 12-MHAcan inhibit the (Z)-9desaturation of El 1-l4:Acid by themselves

Objectives

Methods

Conclusion