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Phytophthora blight of pepper caused by Phytophthora capsici Leonian is a destructive disease throughout the world. Cuminic acid, extracted from the seed of Cuminum cyminum L., belongs to the benzoic acid chemical class. In this study, the sensitivity and biochemical response of P. capsici to cuminic acid was determined. The mean EC 50 (50% effective concentration) values for cuminic acid in inhibiting mycelial growth and zoospore germination of the 54 studied P. capsici isolates were 14.54˘5.23 µg/mL and 6.97˘2.82 µg/mL, respectively. After treatment with cuminic acid, mycelial morphology, sporangium formation and mycelial respiration were significantly influenced; cell membrane permeability and DNA content increased markedly, but pyruvic acid content, adenosine triphosphate (ATP) content, and ATPase activity decreased compared with the untreated control. In pot experiments, cuminic acid exhibited both protective and curative activity. Importantly, POD and PAL activity of the pepper leaves increased after being treated with cuminic acid. These indicated that cuminic acid not only showed antifungal activity, but also could improve the defense capacity of the plants. All the results suggested that cuminic acid exhibits the potential to be developed as a new phytochemical fungicide, and this information increases our understanding of the mechanism of action of cuminic acid against Phytophthora capsici.

The potential use of allyl isothiocyanate (AITC) and ethyl isothiocyanate (EITC), singly and in combination, was tested in in vitro and in vivo trials for their effect on Penicillium expansum Link and Botrytis cinerea Persl. infection on apple when used as a fumigant. A 3 : 1 ratio of AITC : EITC was more efficient at reducing in vitro spore germination of P. expansum and B. cinerea than were other combinations or either AITC or EITC alone. The optimized combination showed the lowest EC 50 values, at 0.08 and 0.14 lg ⁄ ml air, for P. expansum conidial germination and mycelial growth, respectively, and 0.07 and 0.12 lg ⁄ ml air for B. cinerea conidial germination and mycelial growth, respectively. In in vivo trials, artificially infected apples were exposed for 4 days to an ITC-enriched atmosphere. Among the ITCs tested, AITC, EITC and their combinations reduced incidence by more than 85% after 3-4 days of apple incubation at 20°C. Although further studies are necessary to evaluate any detrimental effects on apple quality, the evidence from this study supports the use of fumigation based on ITCs, and in particular a 3 : 1 combination of AITC and EITC, for control of postharvest mildew in apple fruit.

Although dietary α-linolenic acid (ALA) or linolenic acid (LA) intake was reported to be epidemiologically associated with a lower prevalence of hypertension, recent clinical trials have yielded conflicting results. Comparable experimental evidence for the roles of these two different fatty acids is still lacking and the underlying mechanisms need to be further elucidated. Our data showed that ALA but not LA supplementation alleviated systolic blood pressure elevation and improved ACh-induced, endothelium-dependent vasodilation in both spontaneously hypertensive rats (SHRs) and AngII-induced hypertensive mice. In addition, SHRs displayed reduced vascular Sirtuin 3 (SIRT3) expression, subsequent superoxide dismutase 2 (SOD2) hyperacetylation and mitochondrial ROS overproduction, all of which were ameliorated by ALA but not LA supplementation. In primary cultured endothelial cells, ALA treatment directly inhibited SIRT3 reduction, SOD2 hyperacetylation, mitochondrial ROS overproduction and alleviated autophagic flux impairment induced by AngII plus TNFα treatment. However, these beneficial effects of ALA were completely blocked by silencing SIRT3. Restoration of autophagic flux by rapamycin also inhibited mitochondrial ROS overproduction in endothelial cells exposed to AngII plus TNFα. More interestingly, SIRT3 KO mice developed severe hypertension in response to a low dose of AngII infusion, while ALA supplementation lost its anti-hypertensive and endothelium-protective effects on these mice. Our findings suggest that ALA but not LA supplementation improves endothelial dysfunction and diminishes experimental hypertension by rescuing SIRT3 impairment to restore autophagic flux and mitochondrial redox balance in endothelial cells.

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