RESUMEN
UPLC-MS/MS and GC-MS/MS were used to establish a method to simultaneously determine various pesticide residues in Panax notoginseng. Results showed that the limits of detection of 249 pesticides were all 5-10 µg/kg. The detection rate of pesticides in 121 P. notoginseng samples was 93.39%, and 19 pesticides were detected. According to the US Code of Federal Regulations, the Chinese Pharmacopoeia recommended algorithm, and the Japanese "positive list system", the pass rates of pesticide residues were 100%, 99.17%, and 89.26%, respectively. The chronic risk quotient (ADI%) and acute risk quotient (ARfD%) of P. notoginseng were 0.00-0.12% and 0.00-0.15%, respectively. In summary, the detection method established in this study can be used for routine analysis of various P. notoginseng pesticide residues. The pesticide residues in the main root samples of P. notoginseng were at a safe level and unlikely pose health risks to consumers.
Asunto(s)
Panax notoginseng , Residuos de Plaguicidas , Cromatografía Liquida , Ingestión de Alimentos , Contaminación de Alimentos/análisis , Panax notoginseng/química , Residuos de Plaguicidas/análisis , Medición de Riesgo , Espectrometría de Masas en Tándem/métodosRESUMEN
With the goal of cost-effective and high-efficient microalgae-based biodiesel production, this study evaluated the feasibility of the joint strategy concerning myo-inositol (MI) and salinity stress on lipid productivity of Monoraphidium sp. QLY-1 in molasses wastewater (MW). The maximal lipid productivity (147.79 mg L-1 d-1) was obtained under combined 0.5 g L-1 MI and 10 g L-1 NaCl treatment, which was 1.40-fold higher than the control. Meanwhile, the nutrients removal from MW was markedly increased under MI-NaCl treatment. Moreover, exogenous MI upregulated key lipogenic genes' expressions, activated autophagic activity and ethylene (ET) signaling, and ultimately alleviated the salinity-induced damage via reactive oxygen species (ROS) signaling. Further pharmacologic experiment confirmed the indispensable role of ET in the lipogenesis progress under the combined treatment. These data demonstrated the combined salinity stress and MI treatment to be capable for lipid hyperproduction and wastewater nutrients removal, which contributes to practically integrating the microalgae cultivation with wastewater treatment.
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Microalgas , Biocombustibles , Biomasa , Etilenos/metabolismo , Inositol/metabolismo , Lípidos , Microalgas/metabolismo , Melaza , Salinidad , Aguas ResidualesRESUMEN
A major challenge facing by astaxanthin industrialization is the low productivity and high production costs. This study established a two-stage cultivation strategy based on the application of NaCl to improve the production of biomass and astaxanthin by Haematococcus pluvialis. During the first growth stage, 12.5 mg L-1 NaCl led to a remarkable enhancement in biomass, which was 1.28 times compared with the control. Moreover, 2 g L-1 NaCl stimulated the astaxanthin content from 12.18 mg g-1 to 25.92 mg g-1 during the second induction stage. Simultaneously, salinity stress application increased the lipids and GABA contents, as well as the levels of Ca2+ and carotenogenic genes' expression, but suppressed the contents of carbohydrate and protein and high-light induced-ROS. This study proposed a simple and convenient strategy for efficient coproduction of biomass and astaxanthin and provides insights into the underlying mechanism of astaxanthin biosynthesis in H. pluvialis induced by salinity stress.
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Chlorophyceae , Cloruro de Sodio , Biomasa , Cloruro de Sodio/farmacología , XantófilasRESUMEN
Haematococcus pluvialis is a commercial microalgae used for natural astaxanthin production. This study aims to investigate the roles of melatonin (MT) and 3-methyladenine (3-MA) in regulating the cell growth and biosynthesis of astaxanthin and fatty acids under adverse conditions by H. pluvialis. Upon the dual treatments, the maximum astaxanthin concentration (46.78 mg L-1) was 2.39- and 1.35-fold higher compared with the control and MT treatments, respectively. Concomitantly, the combined application of MT and 3-MA suppressed autophagy but promoted the production of biomass and lipids and upregulated carotenogenesis, lipogenesis and antioxidant enzyme-related genes at the transcriptional level, which were linked with astaxanthin and lipid biosynthesis and oxidative stress. Additionally, astaxanthin exhibited a noticeable increase under MT coupled with 3-MA in the other two strains of H. pluvialis. This study proposed a potential method for astaxanthin induction and provided insights into the function of autophagy in modulating cell growth and astaxanthin synthesis.
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Chlorophyceae , Melatonina , Adenina/análogos & derivados , Biomasa , XantófilasRESUMEN
This study focused on the influence of integrating melatonin (MT) and calcium (Ca2+) on the simultaneous accumulation of astaxanthin and lipids in Haematococcus pluvialis under abiotic stress conditions. Compared with the control condition, MT induction enhanced astaxanthin and lipid contents by 65.89% and 27.38%, respectively. The highest contents of astaxanthin and lipids under combined exposure to MT and Ca2+ were 3.8% and 49.53%, respectively, which were 1.13- and 1.21-fold higher than those of cells treated with MT alone. The application of MT and Ca2+ also promoted the expression of carotenogenic and lipogenic genes and increased the levels of Ca2+ and γ-aminobutyric acid (GABA) but decreased reactive oxygen species (ROS) levels. Further evidence indicated that the increased cellular Ca2+ could promote astaxanthin biosynthesis under MT induction by regulating carotenogenic gene levels and GABA and ROS signalling. The integrated strategy efficiently improved the coproduction of astaxanthin and lipids in H. pluvialis.
RESUMEN
This study explored the effects of γ-aminobutyric acid (GABA) on the production of biomass and lipids and on the uptake of Cd2+ by microalgae under cadmium (Cd) stress. Compared with the control and Cd stress alone, 2.5 mM GABA increased the maximum lipid content (55.37%) by 49.37% and 9.42%, respectively. GABA application resulted in increased contents of protein and glutathione (GSH) and in upregulated activity of α-amylase but decreased contents of starch, reactive oxygen species (ROS) and Cd2+, with no effect on subsequent biodiesel quality. Additional analysis of GABA further indicated that increased cellular GABA contents could promote lipid synthesis and reduce Cd accumulation by regulating the expression levels of lipogenesis genes, ROS signalling and mineral nutrient uptake under Cd stress. Collectively, these findings show that GABA not only increases lipid production in microalgae but also is involved in the mechanisms by which microalgae respond to Cd stress.
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Cadmio , Microalgas , Biomasa , Lípidos , Ácido gamma-AminobutíricoRESUMEN
Purpose: The aim of this study was to explore the mechanism of neurological changes underlying the toxicity of nicotine.Materials and methods: Rat pheochromocytoma 12 (PC12) cells and human neuroglia (HM) cells were used. The ROS levels of the cells were detected by the FACScan. Autophagy flux was monitored by a tandem monomeric RFP-GFP-tagged LC3 lentivirus. The autophagic proteins LC3, SQSTM1/p62 and Beclin1 were detected by western blot assay. In order to evaluate the effects of nicotine and melatonin on the morphological changes of neurons, primary cortical neurons were obtained and immunocytochemistry of TUBB3 tubulin were conducted.Results: Nicotine increased the levels of reactive oxygen species (ROS) in PC12 and HM cells in a concentration-dependent manner. Microscopy showed increased autophagic flux in nicotine-treated PC12 cells. Subsequent western blotting results showed that nicotine induced increase in the levels of LC3B-II and Beclin1, and decreased SQSTM1/p62 in a concentration-dependent manner. Finally, nicotine treatment reduced the length of TUBB3-positive axons and dendrites. Melatonin, a mitochondrially targeted antioxidant, reduced the ROS level, and blocked autophagy activation and the morphologic structural changes induced by nicotine.Conclusions: Our results suggested that the role of nicotine in neuronal toxicity maybe through the induction of ROS and the subsequent activation of autophagy. These effects could be restored by melatonin.