The aryloxyphenoxypropionate and cyclohexanedione herbicides, which inhibit acetyl-coenzyme A carboxylase (EC 6.4.1.2), have also been hypothesized to act at specific sites on the plasmalemma. An impermeant sulfhydryl binding agent was reported to block the diclofop acid-induced depolarization of the membrane potential (Em) in rigid ryegrass. A correlation between the antagonistic interaction with auxin herbicides both in the field and in the Em response, and the repolarization of Em in herbicide-resistant rigid ryegrass following removal of diclofop acid also provide support for this hypothesis. However, similar membrane responses in resistant grasses and broadleaf species suggest that the membrane response may not be important in the phytotoxic activity of the postemergence graminicides under field conditions. In addition, an antagonistic interaction was not observed in roots of susceptible grasses exposed to combinations of diclofop-methyl and 2,4-D. Furthermore, the repolarization of the Em in diclofop-resistant rigid ryegrass was correlated to differential acidification of the external solution and an increase in the protonated form of diclofop acid, rather than a site-specific interaction at the plasmalemma. Although the membrane response is probably not involved in herbicide phytotoxicity in agricultural systems, a higher extracellular pH in the resistant biotypes of rigid ryegrass may inhibit the movement of these weak-acid herbicides across the plasmalemma, and possibly contribute to increased herbicide tolerance.

Effects of a crude preparation of a phytotoxin from Pseudomonas fluorescens strain D7 (D7) on various physiological processes were evaluated in roots of downy brome seedlings. Cell division, respiration, and synthesis of protein, RNA, and DNA were not inhibited or only slightly inhibited under treatment conditions that caused substantial inhibition of root elongation. Significant inhibition of each of these processes was detected by known inhibitors included in each study to verify sensitivity of the procedures used. Disruption of lipid synthesis and membrane integrity by the crude phytotoxin preparation was significant and might account for inhibition of root elongation. Additional studies on these two possible target sites were conducted with partially purified phytotoxin. In intact roots, incorporation of [14C]acetate and [14C]malonic acid into lipophilic fractions was reduced by 50% or greater during a 1-h treatment with concentrations between 10 and 100 μg ml−1 of the partially purified phytotoxin preparation. In a membrane integrity study, a similar treatment increased radioactivity efflux 250% from seedlings preloaded with scyllo-[R-3H]inositol. Additionally, disruption of lipid synthesis and membrane integrity by the partially purified phytotoxin was dose dependent. Collectively, these findings indicate that the D7 phytotoxin may inhibit downy brome root elongation through its effects on lipid synthesis and membrane integrity.

In laboratory experiments, the effects of the herbicides HOE-39866 [ammonium (3-amino-3-carboxypropyl)-methylphosphinate] and SC-0224 (trimethylsulfonium carboxymethylaminomethylphosphonate) on the incorporation of NaH14CO3, [14C]-leucine, [14C]-uracil, and [14C]-acetate into enzymatically isolated soybean [Glycine max (L.) Merr. ‘Essex’] cells were evaluated to assess the activity of these herbicides on CO2 fixation, protein, ribonucleic acid (RNA), and lipid syntheses. At low concentrations neither compound exhibited rapid or distinct inhibitions of any process as might be expected in the case of inhibition of a primary target site. Photosynthesis was the process least affected. At equimolar concentrations, protein and RNA syntheses were more sensitive to HOE-39866 than to SC-0224 while the reverse occurred in lipid synthesis. Protein synthesis appears to be a possible target site that may be involved in the herbicidal action of these two compounds.

In addition to its economic value, milk fat is responsible for many of milk’s characteristics and can be markedly affected by diet. Diet-induced milk fat depression (MFD) was first described over a century ago and remains a common problem observed under both intensive and extensive management. The biohydrogenation theory established that MFD is caused by an inhibition of mammary synthesis of milk fat by specific fatty acids (FA) produced as intermediates in ruminal biohydrogenation. During MFD, lipogenic capacity and transcription of key lipid synthesis genes in the mammary gland are down-regulated in a coordinated manner. Our investigations have established that expressions of sterol response element-binding protein 1 (SREBP1) and SREBP-activation proteins are down-regulated during MFD. Importantly, key lipogenic enzymes are transcriptionally regulated via SREBP1. Collectively, these results provide strong evidence for SREBP1 as a central signaling pathway in the regulation of mammary FA synthesis. Spot 14 is also down-regulated during MFD, consistent with a lipogenic role for this novel nuclear protein. In addition, SREBP1c and Spot 14 knock-out mice exhibit reduced milk fat similar to the magnitude and pattern of MFD in the cow. Application of molecular biology approaches has provided the latest chapter in the regulation of milk fat synthesis and is reviewed along with a brief background in nutritional regulation of milk fat synthesis in ruminants.

The purpose of the present study was to estimate whole-body fatty acid and cholesterol synthesis in weight-stable adults and to determine the likely effect on the doubly-labelled water (DLW) method for measuring energy expenditure. Synthesis was measured by 2H incorporation over 14 d in six adult males in approximate energy balance following noradrenaline infusion to maximize mobilization of free fatty acid from adipose tissue. The inter-individual variation in synthesis rates was large and in one subject the proportion of free fatty acid synthesized was ten times that of the mean of the rest of the group; the fasting concentration of esterified fatty acid in this subject was five times that of the rest of the group indicating likely violation of the assumptions underlying the calculation of whole-body synthesis. After 14 d of labelling in the other five subjects, 0·9 (SEM 0·3) % OF THE CIRCULATING FREE FATTY ACID, 9·3 (sem 3·0) % of the esterified fatty acid, 14·6 (sem 2·4) % of the free cholesterol and 28·3 (sem 3·7) % of esterified cholesterol had been synthesized de novo. A high rate of synthesis correlated with a low pre-dose 2H abundance both within and between lipid classes suggesting that natural 2H abundance variations in some lipid classes may be used to determine their metabolic origin. Whole-body synthetic rates were 8 g/d for fatty acid and 0·3–0·5 g/d for cholesterol. These values correspond to very small errors on DLW-derived estimates of CO2 production; -2·5 litres/d for fatty acid and -0·1 to -0·2 litres/d for cholesterol. These results, obtained in subjects typically consuming a diet with a lower fat and cholesterol content that the typical Western diet, suggest that the DLW method is unlikely to be affected by fatty acid and cholesterol synthesis in subjects in energy balance consuming a typical Western diet.