Impact of Postharvest Nitric Oxide Treatment on Lignin Biosynthesis-Related Genes in Wax Apple (Syzygium samarangense) Fruit.

The role of nitric oxide (NO) during storage in wax apple through NO (10 µL/L) fumigate fruit was investigated. Wax apple fruit treated with NO had a significantly lower rate of weight loss, a softening index, and loss of firmness during storage. The transcriptional profile of 10 genes involved in lignin biosynthesis has been analyzed using quantitative real-time polymerase chain reaction (qRT-PCR). The qRT-PCR analysis showed nine genes regulated in the wax apple (p < 0.05) upon NO fumigation, which coincided with the enzyme activity results (NO group lower than control group in peroxidase, phenylalanine ammonia-lyase, and 4-coumarate-CoA ligase), whose total lignin content decreased upon treatment with NO. These results indicate that NO treatment can effectively delay the softening and senescence of wax apple fruit and play an important regulatory role in lignin biosynthesis.

[The SERS Detection of Sudan I by Using AAO as Template to Prepare the Substrate].

The large-scale controllable, ordered two-dimensional arrays of gold nanostructure with hot-spot were prepared together with chemical molecules were modified on the surface to concentrate Sudan I within the zone of the SERS effect, which lead to analytical detection of Sudan I in high resolution. The vapor of gold was deposed on anodic aluminum oxide(AAO) template by -200 nm thickness to replicate its nanochannels, and the negative structure i. e. large-scale ordered gold nano-hemisphere array, was obtained after the removal of the template of AAO by NaOH solution. Au nano-hemisphere array was modified by 1-Dodecanethiol which can be self-assembled monolayer on the surface and concentrate Sudan I within the zone of the SERS detection, which can facilitate the measurement of Sudan I. Due to the order and regularity of Au nano-hemisphere array, the signal of Sudan I in the range of laser illumination is stable and uniform, and the quantitative analysis of Sudan I was realized. The SERS intensity of Sudan I is logistic proportional to the concentration in the range of 10(-7) to 5 x 10(-4) mol x L(-1). The corresponding correlation coefficient of the liner equation is 0.99, the recoveries of Sudan I are between 77% - 117%. The limit of detection for Sudan I is 4 x 10(-1) mol x L(-1), comparable to that of HPLC of Chinese national standard method.

Apoptosis induced by acrylamide is suppressed in a 21.5% fat diet through caspase-3-independent pathway in mice testis.

This study investigates the simultaneous effect of acrylamide (ACR) and high-fat-intake on the apoptosis in testis cells, and also the expression and activity of caspase-3. Seventy-two male Kunming mice were divided into two blocks and fed with a high-fat diet (crude fat 21.5%) or basic diet (crude fat 4.4%), respectively; and animals in each diet block were exposed to ACR at the dose of 20 mg/kgbw x d or 40 mg/kgbw x d as ACR treated groups or the normal saline as control. Germ cells prepared from testis were stained with Hoechst dye 33258 and paraffin wax sections from testis were suffered to a TUNEL process. Expression of caspase-3 on protein level was investigated using an immunohistochemical analysis assay. The supernatant of unilateral testes were subjected to a Caspase-3 activity kit to determine the activity of Caspase-3 in testis. The concentration of ACR and glycidamide(GA), epoxide of ACR, in plasma and testis were detected by LC-ES/MS/MS analysis. Results based on the morphological changes, percentage of apoptotic cells, and integrated optical density (IOD) of positive amethyst staining which indicates the apoptotic DNA fragmentation, show that apoptosis was induced by acrylamide only; however, acrylamide-induced apoptosis was weakened by high-fat-intake. The protein expression and activity of Caspase-3 were not induced by ACR or high-fat-intake. Moreover, no significant differences of ACR and GA concentration were found between the high-fat and basic diet groups after exposure of ACR. Results indicate that high-fat-intake reverses the effects on apoptosis induced by ACR; and more possibly, apoptosis is induced by a caspase-3-independent mechanism.