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This paper assessed the antifungal effects of sage oil, lavender oil, mint oil, and tea tree oil on the postharvest fungal pathogen, Botrytis cinerea, which causes gray molds. The change of morphology, physiological, and biochemical characteristics about fungal hyphae and conidia were determined. As results show, all four oils can effectively inhibit the growth of B.cinerea and the antifungal effects are dose dependent. The best antifungal effect has been found from mint oil. According to in vitro studies, volatile vapor worked better than direct contact. With volatile vapor, the growth of B.cinerea was inhibited completely at 2 for all four oils. Mint oil at 500 μL/L and its volatile vapor at 25 could inhibit both conidia germination and disease incidence significantly in vivo. Observations by using scanning electron microscope and transmission electron microscope revealed that, mint oil could destroy the ultrastructure of hyphae and conidia, resulting in markedly shriveling and crinkling of the hyphae and conidia. It could also thicken and disrupt cell wall, causing cellular nucleic acids and proteins divulged with the damage of the cell wall. The chemical composition analysis of mint oil using GC/MS revealed that its main components were cyclohexanol, cyclohexanone, and some alkenes and alkanes. The majority of the components were effective antifungal agents. The content of volatile cyclohexanol and cyclohexanone were found to be 39.79% and 22.24% respectively.

Fucoidan, the complex fucose-containing sulphated polysaccharide varies considerably in structure, composition, and bioactivity, depending on the source, species, seasonality, and extraction method. In this study, we examined five fucoidans extracted from the same seaweed species Undaria pinnatifida but from different geological locations, and compared them to the laboratory-grade fucoidan from Sigma (S). The five products differed in molecular composition. The amount of over 2 kDa low molecular weight fraction (LMWF) of the New Zealand crude fucoidan (S1) was larger than that of S, and this fraction was unique, compared to the other four fucoidans. The difference of molecular compositions between S and S1 explained our previous observation that S1 exhibited different anticancer profile in some cancer cell lines, compared with S. Since we observed this unique LMWF, we compared the cytotoxic effects of a LMWF and a high molecular weight fucoidan (HMWF) in two breast cancer cell lines—MCF-7 and MDA-MB-231. Results indicated that the molecular weight is a critical factor in determining the anti-cancer potential of fucoidan, from the New Zealand U. pinnatifida, as the LMWF exhibited a dose-dependent inhibition on the proliferation of breast cancer cells, significantly better than the HMWF, in both cell lines. A time-dependent inhibition was only observed in the MCF-7. Induction of caspase-dependent apoptosis was observed in the MDA-MB-231 cells, through the intrinsic apoptosis pathway alone, or with the extrinsic pathway. LMWF stimulated a dose-dependent NOS activation in the MDA-MB-231 cells. In conclusion, the fucoidan extracted from the New Zealand U. pinnatifida contains a unique LMWF, which could effectively inhibit the growth of breast cancer cell lines. Therefore, the LMWF from New Zealand U. pinnatifida could be used as a supplement cancer treatment.

The effects of a fungal elicitor from Trichothecium roseum on signal pathways of salicylic acid (SA), jasmonic acid (JA), and Ca2+ in potato tubers were investigated. The results showed that fungal elicitor treatment effectively inhibited the lesion diameter of Fusarium sulphureum in vivo, which was 17.5% lower than that of the control. In addition, fungal elicitor treatment triggered an increase in O2− production and H2O2 content. The fungal elicitor enhanced the activities and gene expression levels of isochorismate synthase (ICS), phenylalanine ammonia lyase (PAL), allene oxide cyclase (AOC), allene oxide synthase (AOS), lipoxygenase (LOX), and Ca2+-ATPase. Furthermore, the fungal elicitor promoted an increase in calmodulin (CaM) content. Protective enzymes (dismutase (SOD), catalase (CAT), polyphenol oxidase (PPO), chitinase (CHI), and β-1,3-glucanase (Glu)) and disease-resistance-related genes (PR1, PR2, and PDF1.2) were induced to be upregulated by elicitor treatment. These results indicated that the fungal elicitor induced disease resistance by accelerating the accumulation of reactive oxygen species (ROS), activating SA, JA, and Ca2+ signaling, and upregulating resistance genes. The results of this study revealed the molecular mechanism of fungal elicitor-induced resistance in the potato, which provides a theoretical basis for the mining of new, safe, and efficient elicitor-sourced antifungal agents and is of great importance for the effective control of potato dry rot disease.

Kiwifruit fruit stored at low temperatures are susceptible to chilling injury, leading to rapid softening, which therefore affects storage and marketing. The effect of 150 nM mL−1 of exogenous phytosulfokine α (PSKα) on reactive oxygen species (ROS) metabolism, Ca2+ signaling, and signal-transducing MAPK in kiwifruit, stored at 0 °C for 60 days, was investigated. The results demonstrated that PSKα treatment effectively alleviated chilling injury in kiwifruit, with a 15% reduction in damage compared to the control on day 60. In addition, PSKα enhanced the activities and gene expression levels of superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), glutathione reductase (GR), Ca2+−ATPase, and mitogen−activated protein kinase (MAPK). In contrast, the activities and gene expression levels of NADPH oxidase (NOX) were inhibited, leading to a lower accumulation of O2− and H2O2, which were 47.2% and 42.2% lower than those in the control at the end of storage, respectively. Furthermore, PSKα treatment enhanced the calmodulin (CaM) content of kiwifruit, which was 1.41 times that of the control on day 50. These results indicate that PSKα can mitigate chilling injury and softening of kiwifruit by inhibiting the accumulation of ROS, increasing antioxidant capacity by inducing antioxidant enzymes, activating Ca2+ signaling, and responding to MAPK protein kinase. The present results provide evidence that exogenous PSKα may be taken for a hopeful treatment in alleviating chilling injury and maintaining the quality of kiwifruit.

The author name “Ren Xueuan” should be corrected and read as “Ren Xueyan”.

Black spot, one of the major diseases of kiwifruit, is caused by Alternaria alternata. A comprehensive investigation into its pathogenicity mechanism is imperative in order to propose a targeted and effective control strategy. The effect of L-arginine on the pathogenicity of A. alternata and the underlying mechanisms were investigated. The results showed that treatment with 5 mM L−1 of L-arginine promoted spore germination and increased the colony diameter and lesion diameter of A. alternata in vivo and in vitro, which were 23.1% and 9.3% higher than that of the control, respectively. Exogenous L-arginine treatment also induced endogenous L-arginine and nitric oxide (NO) accumulation by activating nitric oxide synthase (NOS), arginine decarboxylase (ADC) and ornithine decarboxylase (ODC). In addition, exogenous L-arginine triggered an increase in reactive oxygen species (ROS) levels by activating the activity and inducing gene expression upregulation of NADPH oxidase. The hydrogen peroxide (H2O2) and superoxide anion (O2.−) levels were 15.9% and 2.2 times higher, respectively, than in the control group on the second day of L-arginine treatment. Meanwhile, antioxidant enzyme activities and gene expression levels were enhanced, including superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), glutathione peroxidase (GPX), and glutathione reductase (GR). In addition, exogenous L-arginine stimulated cell wall-degrading enzymes in vivo and in vitro by activating gene expression. These results suggested that exogenous L-arginine promoted the pathogenicity of A. alternata by inducing the accumulation of polyamines, NO, and ROS, and by activating systems of antioxidants and cell wall-degrading enzymes. The present study not only revealed the mechanism by which low concentrations of L-arginine increase the pathogenicity of A. alternata, but also provided a theoretical basis for the exclusive and precise targeting of A. alternata in kiwifruit.

Xinjiang wine grapes (Vitis Vinifera) are extraordinarily rich sources of stilbenes. In this study, two pair of isomers of resveratrol dimers trans-ε-viniferin (1) and (+)-cis-ε-viniferin (2), astilbin (4) and isoastilbin (5), and resveratrol tetramer (−)-hopeaphenol (3) were isolated and purified. Their structures were determined by means of nuclear magnetic resonance and mass spectrometry analysis. Then, cellular antioxidant activity of the five phenolic compounds was evaluated in human hepatoma (Hep G2) cells. Results indicated that (4) has the strongest antioxidant activity (10 µg/mL), while (5) is the weakest one. Mechanism process of antioxidant at genes expression was elaborated by real-time quantitative PCR, which showed that the five stilbenes could down-regulation of oxidative stress genes and apoptosis genes. Therefore, this study provides the useful evidence for these compounds to develop the functional foods and nutritional supplements.Graphical abstractFive phenolic compounds, trans-ε-viniferin (1) and (+)-cis-ε-viniferin (2), astilbin (4) and isoastilbin (5), resveratrol tetramer (−)-hopeaphenol (3) were isolated and purified. These five compounds have a significantly reduced effect on oxidative stress genes at cellular level by real-time quantitative PCR

Fucoidan, a sulfated polysaccharide extracted from brown seaweeds, has been shown to possess various antioxidant, anticoagulant, antiviral, and anticancer functions. In this study, we focused on low molecular weight fucoidan (LMWF) which was extracted from New Zealand Undaria pinnatifida, and investigated its anti-proliferative effects, combined with a quadruplex-forming oligonucleotide aptamer (GroA, AS1411), a powerful cell surface Nucleolin inhibitor, in prostate cancer cells. We examined LMWF (<10 kDa) and compared it with laboratory grade Fucoidan purchased from Sigma (FS), all extracted from the same seaweed species U. pinnatifida. We found that LMWF significantly improved the anti-proliferative effect of GroA, as it decreased cancer cell growth and viability and increased cell death. This research may provide the foundation for LMWF to be used against prostate cancers as a supplement therapy in combination with other therapeutic agents.

Black spot caused by Alternaria alternata is one of the most common postharvest diseases in fruit and vegetables. A comprehensive investigation into its pathogenicity mechanism is imperative in order to propose a targeted and effective control strategy. The effect of nitric oxide (NO) on the pathogenicity of A. alternata and its underlying mechanism was studied. The results showed that treatment with 0.5 mM L−1 of sodium nitroprusside (SNP) (NO donor) increased the lesion diameter of A. alternata in vivo and in vitro, which was 22.8% and 13.2% higher than that of the control, respectively. Exogenous NO treatment also induced endogenous NO accumulation by activating nitric oxide synthase (NOS). In addition, NO triggered an increase in reactive oxygen species (ROS) levels. NO enhanced activities and gene expression levels of NADPH oxidase (NOX), superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), glutathione peroxidase (GPX), and glutathione reductase (GR). Moreover, NO stimulated cell wall degrading enzymes by activating the corresponding gene expression in vivo and in vitro. These results suggested that exogenous NO promoted the pathogenicity of A. alternata by inducing ROS accumulation and activating antioxidants and cell wall degrading enzymes. The present results could establish a theoretical foundation for the targeted control of the black spot disease in pear fruit.

Stilbenes, particularly resveratrol and resveratrol dimers, could effectively quench singlet oxygen (1O2). It was reported that both resorcinol and carbon-carbon double bond quenching 1O2 can participate in the mechanism. However, it is still not clear which structure plays a dominant role in quenching 1O2. To investigate the characteristic structure in the mechanism of quenching 1O2, the resveratrol, pterostilbene and piceatannol quenching 1O2 abilities were compared by UHPLC-QTOF-MS2 and UHPLC-QQQ-MS2. Results showed that catechol, carbon-carbon double bond and resorcinol participated in the quenching of 1O2. Catechol ring plays a leading role in the mechanism, and the contribution of the structures in quenching 1O2 activity are as follows: catechol ring > carbon-carbon double bond > resorcinol ring, which is supported by the calculation of energy. Our findings will contribute to the future screening of stilbenes with higher activity, and those stilbenes may have great therapeutic potential in 1O2-mediated diseases.