Phomopsis longanae Chi causing the pulp breakdown of fresh longan fruit through affecting reactive oxygen species metabolism.

Phomopsis longanae Chi is a crucial pathogen causing fruit spoilage in postharvest fresh longan. The influence of P. longanae invasion with a suspension containing 1 × 104 P. longanae spores per mL on the breakdown occurrence and ROS metabolism in pulp of longan cv. Fuyan during storage at 28 °C was explicated. Compared to control group, more severe development of pulp breakdown (PB), higher PB index, O2 -. generation rate, H2O2 and MDA content, but lower SOD, APX and CAT activities, GSH, AsA, flavonoid and total phenolics amounts, ability of scavenging DPPH radical, and reducing power were displayed in the pulp of P. longanae-infected fruit during days 0-5. In this context, P. longanae induced breakdown of longan pulp by reducing the scavenging ability of ROS and increasing the cumulation of ROS, thereby enhancing the structural collapse and lipid peroxidation of cell membrane, which were responsible for the PB of harvested longans.

DNP and ATP regulate the pulp breakdown development in Phomopsis longanae Chi-infected longan fruit through modulating the ROS metabolism.

Compared with the P. longanae-infected longan, the DNP-treated P. longanae-infected fruit represented a higher pulp breakdown index, a higher O2 -. production rate, and a higher MDA content, but the lower activities of APX, SOD and CAT, the lower transcript levels of DlAPX6, DlSOD1, DlSOD2, DlSOD3 and DlCAT1, the lower values of AsA, GSH, flavonoid and total phenolics, a lower scavenging ability of DPPH radical, and a lower value of reducing power. Whereas, the ATP-treated P. longanae-infected samples showed the contrary results. The above findings indicated that the DNP-promoted the pulp breakdown in P. longanae-infected longan was because DNP weakened the capacity of scavenging ROS, raised the O2 -. level, and accelerated the membrane lipids peroxidation. However, the ATP-suppressed the pulp breakdown in P. longanae-infected longan was because ATP improved the capacity of scavenging ROS, reduced the O2 -. level, and reduced the membrane lipids peroxidation.

Physiological and biochemical analysis of mechanisms underlying cadmium tolerance and accumulation in turnip.

The capacity of plants to accumulate cadmium (Cd) is significant for phytoremediation of Cd-polluted soils. Turnips cultivated in China include species featuring high Cd accumulation and some of these plants act as Cd hyperaccumulator landraces. These plants can accumulate over 100 mg Cd kg-1 dry weight in leaves without injury. Hence, studies that explore mechanisms underlying Cd detoxification and transport in turnip plants are essential. In the present study, we compared physiological and biochemical changes in turnip leaves treated with two Cd concentrations to controls. We discovered that Cd stress significantly increased the enzymatic activities or compound contents in the antioxidant system, including members of the glutathione-ascorbic acid cycle, whereas oxidation of reactive oxygen species (ROS) remained stable. Cd treatments also increased the contents of phytochelatins as well as a number of amino acids. Based on these results, we conclude that turnips initiate a series of response processes to manage Cd treatment. First, the antioxidant system maintaining ROS homeostasis and osmotic adjustment is excited to maintain stability of cell osmotic potential. Cd is chelated into its stable form to reduce its toxicity. Cd is possibly transported to vacuoles or non-protoplasts for isolation. Amino acid synthesis may directly and indirectly play an important role in these processes. This study partly revealed physiological and biochemical mechanisms underlying turnip response to Cd stress and provides information on artificially increasing or decreasing Cd accumulation in turnips and other plants.

Computational Modeling of Oxidative Stress in Fatty Livers Elucidates the Underlying Mechanism of the Increased Susceptibility to Ischemia/Reperfusion Injury.

QUESTION: Donor liver organs with moderate to high fat content (i.e. steatosis) suffer from an enhanced susceptibility to ischemia/reperfusion injury (IRI) during liver transplantation. Responsible for the cellular injury is an increased level of oxidative stress, however the underlying mechanistic network is still not fully understood. METHOD: We developed a phenomenological mathematical model of key processes of hepatic lipid metabolism linked to pathways of oxidative stress. The model allows the simulation of hypoxia (i.e. ischemia-like conditions) and reoxygenation (i.e. reperfusion-like conditions) for various degrees of steatosis and predicts the level of hepatic lipid peroxidation (LPO) as a marker of cell damage caused by oxidative stress. RESULTS & CONCLUSIONS: Our modeling results show that the underlying feedback loop between the formation of reactive oxygen species (ROS) and LPO leads to bistable systems behavior. Here, the first stable state corresponds to a low basal level of ROS production. The system is directed to this state for healthy, non-steatotic livers. The second stable state corresponds to a high level of oxidative stress with an enhanced formation of ROS and LPO. This state is reached, if steatotic livers with a high fat content undergo a hypoxic phase. Theoretically, our proposed mechanistic network would support the prediction of the maximal tolerable ischemia time for steatotic livers: Exceeding this limit during the transplantation process would lead to severe IRI and a considerable increased risk for liver failure.

Coenzyme Q10 prevents accelerated cardiac aging in a rat model of poor maternal nutrition and accelerated postnatal growth.

Studies in human and animals have demonstrated that nutritionally induced low birth-weight followed by rapid postnatal growth increases the risk of metabolic syndrome and cardiovascular disease. Although the mechanisms underlying such nutritional programming are not clearly defined, increased oxidative-stress leading to accelerated cellular aging has been proposed to play an important role. Using an established rodent model of low birth-weight and catch-up growth, we show here that post-weaning dietary supplementation with coenzyme Q10, a key component of the electron transport chain and a potent antioxidant rescued many of the detrimental effects of nutritional programming on cardiac aging. This included a reduction in nitrosative and oxidative-stress, telomere shortening, DNA damage, cellular senescence and apoptosis. These findings demonstrate the potential for postnatal antioxidant intervention to reverse deleterious phenotypes of developmental programming and therefore provide insight into a potential translatable therapy to prevent cardiovascular disease in at risk humans.