Study Indicates GliSODin® Shown to Inhibit Surgery-Related Cellular DNA Damage

MORRISTOWN, NJ (February 5, 2007) P.L. Thomas (PLT) today, in association with Isocell, Paris, France, announced the results of a new study using their exclusive dietary supplement ingredient, GliSODin® in the journal of Intensive Care Medicine1. GliSODin supplementation prior to an invasive surgical procedure was shown to significantly inhibit several measures of cellular damage, including DNA damage and protection of spinal cord tissues, without negative effects or impairing organ function.

The researchers were positive in their findings, stating that in this study the use of GliSODin "may thus be an adjunctive measure for elective surgery and / or used as nutritional support under conditions of prolonged period of enhanced oxidative stress."

Invasive surgery interrupts and reintroduces blood flow to tissues causing cellular and tissue damage by reactive oxygen species (ROS). This is called ischemia-reperfusion injury, and the most vulnerable organs are the spinal cord and kidneys. If the cellular DNA and membrane can be protected from ROS, the tissues and organs may be significantly protected and will suffer less damage.

In the study, conducted at the University of Ulm, invasive surgery was modeled by clamping the thoracic aorta for 30 minutes under carefully controlled conditions. GliSODin supplementation for 14 days prior to the procedure was compared to similar supplementation with placebo.

GliSODin was shown to significantly reduce surgery- and Ischemia/repurfusion-related DNA damage and decrease spinal cord cell death. Further, cellular damage typically seen during surgery considered harmful to cardiac function was inhibited (venous acidosis) without limiting normal lipid peroxidation or organ function. No protective benefit was shown in the placebo group.

This new study builds upon previous research in humans. In a double-blind, placebo-controlled clinical trial that was published in Free Radical Research2 (link) , September 2004, the researchers showed GliSODin supplementation protects cellular DNA against induced oxidative damage. GliSODin was the only supplement to show a protective benefit in this well-established model of oxidative stress.

In the new study, swine were chosen for the tests as issues that can influence human studies, such as smoking, dietary habits or exercise are negated. Also, swine are similar to humans in susceptibility to oxidative stress and tissue antioxidant profiles. The study was conducted in accordance to ethical guidelines for animal research.

Previous published human and laboratory studies have shown GliSODin's effectiveness in protecting cells from oxidative stress by activating the body's production of its own antioxidants, including SOD, catalase and glutathione peroxidase.

This "internal antioxidant defense system" is necessary for the elimination of the free radicals produced by oxidative stress, resulting in tangible health benefits, including helping protect cellular DNA from oxidative stress, inhibit photo-oxidative stress in the sun-sensitive, inhibit lactic acid accumulation under exercise, help restore normal levels of SOD, and positively affect other significant markers of oxidative stress.

More information on GliSODin is available at the research site and

Contact PL Thomas: Eric Anderson, phone: 973-984-0900, ext. 214, fax: 973-984-5666, [email protected] or

About GliSODin®

GliSODin is patented and trademarked by Isocell, Paris, France. It is available in North America as a nutritional raw material exclusively from PL Thomas & Co., Morristown, NJ. Numerous in vivo and human studies support the use of GliSODin in nutritional applications.

About PLT

P.L. Thomas, a New Jersey-based ingredient supplier, offers fifty years of innovation in securing reliable, high quality raw materials for the food/functional food and nutrition industries.

1 Kick, et. al., "Effects of a cantaloupe melon extract/wheat gliadin biopolymer during aortic cross-clamping," Journal Intensive Care Medicine 10.1007/s00134-006-0518-6

2 Muth, et. al. "Influence of an orally effective SOD on hyperbaric, oxygen related cell damage," Free Radical Research 38:9 (2004) pp. 927-932

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