Enhancing astaxanthin accumulation through the expression of the plant-derived astaxanthin biosynthetic pathway in Dunaliella salina.

Dunaliella salina, a microalga that thrives under high-saline conditions, is notable for its high ß-carotene content and the absence of a polysaccharide cell wall. These unique characteristics render it a prime candidate as a cellular platform for astaxanthin production. In this study, our initial tests in an E. coli revealed that ß-ring-4-dehydrogenase (CBFD) and 4-hydroxy-ß-ring-4-dehydrogenase (HBFD) genes from Adonis aestivalis outperformed ß-carotene hydroxylase (BCH) and ß-carotene ketolase (BKT) from Haematococcus pluvialis counterparts by two-fold in terms of astaxanthin biosynthesis efficiency. Subsequently, we utilized electroporation to integrate either the BKT gene or the CBFD and HBFD genes into the genome of D. salina. In comparison to wild-type D. salina, strains transformed with BKT or CBFD and HBFD exhibited inhibited growth, underwent color changes to shades of red and yellow, and saw a nearly 50% decline in cell density. HPLC analysis confirmed astaxanthin synthesis in engineered D. salina strains, with CBFD + HBFD-D. salina yielding 134.88 ± 9.12 µg/g of dry cell weight (DCW), significantly higher than BKT-D. salina (83.58 ± 2.40 µg/g). This represents the largest amount of astaxanthin extracted from transgenic D. salina, as reported to date. These findings have significant implications, opening up new avenues for the development of specialized D. salina-based microcell factories for efficient astaxanthin production.

[Uptake and Volatilization of Gaseous Elemental Mercury by Paddy Rice].

Wetlands are important sinks for mercury, and its reducing substrate favors the production of gaseous elemental mercury. In order to adapt to the anoxic condition, wetland plants usually have developed aerenchyma to transfer oxygen from the shoots to the roots to supply their roots respiration. In this study, a typical wetland plant, rice, is used to investigate whether its aerenchyma can also be a channel for the transportation of rhizosphere gaseous mercury into the atmosphere. In addition, the underlying mechanisms will be evaluated. In this study, the roots of rice were separated from the shoots by an air-tight chamber. Roots were exposed to saturated mercury vapor in the root chamber, and the gaseous mercury volatilized from the leaf chamber was absorbed by an active carbon absorbent. The results showed that gaseous elemental mercury could be transferred to shoots after absorption by the roots. The mercury in the roots decreased polynomially with root porosity (R=0.8309, P<0.01), while the mercury in the above ground tissues showed a positive correlation with root surface area and root volume (R=0.896, P<0.01; R=0.871, P<0.01). It was also indicated that the mercury absorbed by the roots could be volatilized into the atmosphere through the leaves. The volatilization of the mercury from the leaves increased positively with the leaf area (R=0.897, P<0.01). There was also a significant positive correlation between the mercury volatilization per unit leaf area and transpiration intensity (R=0.73,P<0.01). The results proved that rice can absorb gaseous elemental mercury through its roots and transfer it above ground for emission into the atmosphere through the stomata of the leaves. This provides a scientific basis for further investigations to reveal mercury behavior and its mechanisms in wetland ecosystems.

Bis(acetylacetonato)-oxidovanadium(IV) and sodium metavanadate inhibit cell proliferation via ROS-induced sustained MAPK/ERK activation but with elevated AKT activity in human pancreatic cancer AsPC-1 cells.

In this study, the antiproliferative effect of bis(acetylacetonato)-oxidovanadium(IV) and sodium metavanadate and the underlying mechanisms were investigated in human pancreatic cancer cell line AsPC-1. The results showed that both exhibited an antiproliferative effect through inducing G2/M cell cycle arrest and can also cause elevation of reactive oxygen species (ROS) levels in cells. Moreover, the two vanadium compounds induced the activation of both PI3K/AKT and MAPK/ERK signaling pathways dose- and time-dependently, which could be counteracted with the antioxidant N-acetylcysteine. In the presence of MEK-1 inhibitor, the degradation of Cdc25C, inactivation of Cdc2 and accumulation of p21 were relieved. However, the treatment of AKT inhibitor did not cause any significant effect. Therefore, it demonstrated that the ROS-induced sustained MAPK/ERK activation rather than AKT contributed to vanadium compounds-induced G2/M cell cycle arrest. The current results also exhibited that the two vanadium compounds did not induce a sustained increase of ROS generation, but the level of ROS reached a plateau instead. The results revealed that an intracellular feedback loop may be against the elevated ROS level induced by vanadate or VO(acac)2, evidenced by the increased GSH content, the unchanged level at the expression of antioxidant enzymes. Therefore, vanadium compounds can be regarded as a novel type of anticancer drugs through the prolonged activation of MAPK/ERK pathway but retained AKT activity. The present results provided a proof-of-concept evidence that vanadium-based compounds may have the potential as both antidiabetic and antipancreatic cancer agents to prevent or treat patients suffering from both diseases.