Clariol, a novel diterpenoid, was isolated from the roots of clary sage (Salvia sclarea L.). The structure was identified as 9-methoxy-2,3-dihydro-4-methyl-8-(1-methylethyl)-2-(2-methyl-2-propenyl)-naphthol[1,8-bc]pyran-3-ol

Two experiments were conducted to determine the effects on male chicken performance of anacardic acid and cashew nut shell oil as feed supplements during an experimental coccidial infection. Seven-day-old chicks wer e fed a corn-soybean diet containing anacardic acid at 0, 0.4 or 0.8% (Experiment 1), or cashew nut shell oil at 0, 0.1, 0.2 or 0.4% (Experiment 2) for 10 days. On the third day of each experiment, half of the birds fed each diet were individually inoculated orally with 2 × 10 3 or 5 × 10 4 (Experiment 1) and 1 × 10 4 or 1 × 10 5 (Experiment 2) Eimeria tenella oocysts. In Experiment 1, body weight gain and cecal length decreased significantly according to the level of oocyst inoculation, while oocyst production per cecum (log value) and cecal lesion score significantly increased. Dietary anacardic acid supplementation had no effect on these parameters except for that of lesion score, which was improved (i.e. decreased) by anacardic acid supplementation of 0.8% at the inoculation level of 2 × 10 3 oocysts, and of 0.4 and 0.8% for the higher inoculation (5 × 10 4 oocysts). Results of Experiment 2 also showed that cashew nut shell oil affected neither cecal length nor oocyst production per cecum (log value) at either of the inoculation levels, but the lesion score was improved by cashew nut shell oil supplementation at 0.2 and 0.4% in the diet at the inoculation level of 1 × 10 4 oocysts and at 0.4% for the higher inoculation. The present study provides the first evidence of the reducing effects of anacardic acid and cashew nut shell oil on the severity of cecal lesions in chickens during an experimental coccidial infection.

We have previously shown that anacardic acid has an uncoupling effect on oxidative phosphorylation in rat liver mitochondria using succinate as a substrate (Toyomizu et al . 2000). In the present study, in order to clarify whether or not anacardic acid could be used advantageously as a special feed/food supplement to reduce fat deposition through the uncoupling action, two sets of experiments were conducted to determine quantitatively the effect of dietary anacardic acid (0.1% w/w) supplementation. More specifically, effects on growth, feed efficiency, fattening, and levels of several constituents of blood serum in rats fed normal and low protein–high carbohydrate (CHO) diets were examined. There were no significant differences in bodyweight gain, feed consumption and feed efficiency among the experimental groups. For the total fat pad content, including inguinal and epididymal fat, significant interaction was shown between both treatments: dietary anacardic acid at 0.1% w/w significantly decreased the total fat pad content in rats fed the CHO diet, but not in rats fed the normal diet. Weights of heart, spleen and brown adipose tissue were not affected by either the dietary treatment or anacardic acid, while both liver and kidney weights decreased with feeding of anacardic acid at 0.1% w/w, but were not affected by the CHO diet. Anacardic acid supplementation in the diet had no effect on serum glutamic oxaloacetic transaminase, alkaline phosphatase or lactate dehydrogenase levels, suggesting that the dysfunction of liver or kidney may not be induced by dietary anacardic acid. The results of the present study reveal a unique function of anacardic acid in that, for dietary conditions enhancing body fat deposition, that is consumption of a diet high in carbohydrates, dietary anacardic acid has the potential to decrease body fat deposition. A possible mechanism for differences observed in anacardic acid-induced regulation of body fat pad content between rats fed the normal and CHO diets, based on uncoupling action of anacardic acid on the mitochondrial oxidative phosphorylation, is discussed.

Anacardic acids are one of natural products found in not only the cashew nut shell oil but also the nut and fruit juice. The present study was conducted to investigate the uncoupling effect of anacardic acids on oxidative phosphorylation of rat liver mitochondria using succinate (plus rotenone) as a substrate. Four anacardic acids with C15:0, C15:1, C15:2 or C15:3 as an alkyl side chain exhibited uncoupling effects similar to the classical uncoupler, 2,4-dinitrophenol on ADP/O ratio, state 4 and respiratory control ratio (RCR). Anacardic acid with C15:1 side chain was most effective for uncoupling of these compounds. Salicylic acid, which has no alkyl side chain, exhibited a very weak uncoupling effect on oxidative phosphorylation. When the carboxyl group in anacardic acids was lost converting them to the corresponding cardanols, uncoupling activity dramatically decreased regardless of the number of double bonds in the long alkyl chain. These results suggest that the C15 alkyl side chain as well as the carboxyl group may play an important role in assisting the uncoupling activity of anacardic acids in liver mitochondria of animals. This study provides the first evidence of an uncoupling effect of anacardic acids on liver mitochondria

A two-part demonstration project is reported which utilized analogous synthesis to reliably deliver a 27-analogue Library which was then evaluated for antioxidative efficiency in a resin-free (ferric thiocyanate assay) deconvolutive assay.