Better broccoli, enhanced anti-cancer benefits with longer shelf life

“Ethylene will move and bind to ethylene receptors and that binding process initiates decay. What this compound does is that it more competitively lands on the protein and binds to or pushes out ethylene,” Juvik explained. “It basically stops or dramatically slows down the decay associated with ethylene.

“The combination is good,” he said.

Like MeJA, 1-MCP is also a non-toxic compound naturally produced in plants, although Juvik said synthetic forms can be produced. He stressed that both the MeJA and 1-MCP treatments required very small amounts of the compounds.

“It’s very cheap, and it’s about as toxic as salt. It takes very little to elevate all the desirable aspects. It’s volatile and disappears from the product after about 10 hours,” he said.

The use of these treatments could make a great impact on important global dilemmas such as food security issues and health-care costs, Juvik said.

Broccoli may help fight cancer by blocking a defective gene associated with tumor growth, according to new research.

Previous studies have heralded the potential cancer-fighting ability of broccoli and other cruciferous vegetables such as cauliflower and watercress. But researchers say until now they didn’t know the secret behind the vegetables’ anticancer attributes.

In a new study, researchers found compounds in broccoli and other cruciferous vegetables called isothiocyanates (ITCs) appear to target and block mutant p53 genes associated with cancer growth.

Gene p53 is known as a tumor suppressor gene and appears to play a critical role in keeping cells healthy and protecting them from cancer. When this gene is damaged or mutated, it stops offering this protection. Researchers say these mutations are found in about half of all human cancers.

In a report published in the Journal of Medicinal Chemistry, researcher Xiantao Wang of Georgetown University and colleagues analyzed the effects of ITCs on gene p53 in a variety of human cancer cells, including lung, breast, and colon cancer, in the lab.

The results showed that ITCs were capable of removing the defective p53 gene while leaving healthy versions of the gene alone.

Researchers say if further studies confirm these findings, it could lead to new therapies for preventing and treating cancer.

“It’s a fairly cheap way to maintain quality, but it provides a preventative approach to all the medical costs associated with degenerative diseases. These are not pills that go in and take away or change damaged tissues, but it’s a way to protect people by reducing the risk they currently have to different diseases. It won’t take it away, but it could prevent further damage,” he said.

As for its impact on impending global food security concerns, Juvik said any mechanisms that will improve people’s health, especially later in life, will benefit food security.

“We need to look at what mechanisms we can use to improve not only food security but the functioning of people later in their life spans. When you look at how much the United States spends on medical costs associated with these diseases, you see it’s a huge burden on the economy, which is the same in all countries. It basically takes away resources that could be used to improve food security,” Juvik said. “Also, promoting and prolonging food stability with quality after harvest means less waste, which is a big issue in terms of food security.”

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“Methyl jasmonate and 1-Methylcyclopropene treatment effects on quinone reductase inducing activity and post-harvest quality of broccoli” was published in the October 2013 issue of Plos One and can be accessed online at http://url.health.am/1398/

Methyl Jasmonate and 1-Methylcyclopropene Treatment Effects on Quinone Reductase Inducing Activity and Post-Harvest Quality of Broccoli

Effect of pre-harvest methyl jasmonate (MeJA) and post-harvest 1-methylcyclopropene (1-MCP) treatments on broccoli floret glucosinolate (GS) concentrations and quinone reductase (QR, an in vitro anti-cancer biomarker) inducing activity were evaluated two days prior to harvest, at harvest and at 10, 20, and 30 days of post-harvest storage at 4 °C. MeJA treatments four days prior to harvest of broccoli heads was observed to significantly increase floret ethylene biosynthesis resulting in chlorophyll catabolism during post-harvest storage and reduced product quality. Post-harvest treatment with 1-methylcyclopropene (1-MCP), which competitively binds to protein ethylene receptors, maintained post-harvest floret chlorophyll concentrations and product visual quality in both control and MeJA-treated broccoli. Transcript abundance of BoPPH, a gene which is responsible for the synthesis of pheophytinase, the primary enzyme associated with chlorophyll catabolism in broccoli, was reduced by 1-MCP treatment and showed a significant, negative correlation with floret chlorophyll concentrations. The GS, glucobrassicin, neoglucobrassicin, and gluconasturtiin were significantly increased by MeJA treatments. The products of some of the GS from endogenous myrosinase hydrolysis [sulforaphane (SF), neoascorbigen (NeoASG), N-methoxyindole-3-carbinol (NI3C), and phenethyl isothiocyanate (PEITC)] were also quantified and found to be significantly correlated with QR. Sulforaphane, the isothiocyanate hydrolysis product of the GS glucoraphanin, was found to be the most potent QR induction agent. Increased sulforaphane formation from the hydrolysis of glucoraphanin was associated with up-regulated gene expression of myrosinase (BoMyo) and the myrosinase enzyme co-factor gene, epithiospecifier modifier1 (BoESM1). This study demonstrates the combined treatment of MeJA and 1-MCP increased QR activity without post-harvest quality loss.
Kang Mo Ku,
Jeong Hee Choi,
Hyoung Seok Kim,
Mosbah M. Kushad,
Elizabeth H. Jeffery,
John A. Juvik

Co-authors of the study were Kang Mo Ku, Jeong Hee Choi, Hyoung Seok Kim, Mosbah M. Kushad, Elizabeth H. Jeffery, and Juvik.

AgroFresh, a division of Rohm & Hass Inc., provided 1-MCP and equipment for the study.


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Jack Juvik
.(JavaScript must be enabled to view this email address)
217-333-1966
University of Illinois College of Agricultural, Consumer and Environmental Sciences

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