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Amazing Superoxide Dismutase SOD - Cancer Cell Treatment

April 12, 2022
Est. Reading: 3 minutes

Superoxide Dismutase (SOD)

As a target for the selective killing of cancer cells, it was published in the U.S. Library of Medicine in 2001 by the Department of Experimental Therapeutics, The University of Texas M.D. Anderson Cancer Center, Houston 77030, USA. Now almost 12 years later, Superoxide Dismutase - SOD is one of the technologies in the invention of the CC Formula as described in several areas of the patent filings.

The principle of the SOD is to dismutate the superoxide anion into molecular oxygen and H2O2. This reaction is catalyzed by the SOD enzymes, which are ubiquitous in biological systems. Most of these enzymes contain metal ions, usually Cu, Zn, or Mn, as cofactors. In addition to their essential role in oxygen metabolism, SOD enzymes are crucial in controlling reactive oxygen species (ROS) and oxidative stress.

sod

The first thing needed to understand the importance of the SOD is some basic information about ROS. Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can damage cells, proteins, and DNA. ROS are produced naturally as a by-product of normal cellular metabolism, but their levels can increase during stress, such as when the body is fighting an infection. Excessive ROS can cause oxidative stress linked to several chronic diseases, including cancer. However, the body has several mechanisms for dealing with ROS, including producing antioxidant enzymes like SOD.

A brief of the recent CC Formula patent continuation on the Copper / Zinc Superoxide Formulation and ALS

Superoxide Dismutase (SOD)

This new application filing is a continuation-ín-part of U.S. application number 11/932,260 (filed October 31, 2007), which is a continuation-in-part of U.S. application number 11/616,317 (filed on December 27, 2006, now abandoned) Which is divisional of U.S. application number 10/027,692 (filed on December 20, 2001, now patent number 7,163,709).

The patent describes the invention of an “artificial” SOD that can be easily applied and used for treating the over-production of superoxide. The disclosed subject concerns chemical composition and treatment methods for ALS patients. A Cu/Zn superoxide dismutase (SOD) neutralizes the debilitating effects suffered by individuals producing excessive superoxide, causing the symptoms of ALS.

The overexpression of the cells toward the manufacture of superoxide links to other neural disorders (e.g., Down syndrome), and the use of the disclosed composition to treat other superoxide-related diseases is also contemplated.

The invention utilizes a new technology directed at a manufacturing process and efficient application of Cu/Zn SOD based on a ligand system. The composition counteracts the effects of the overproduction of superoxide by utilizing a ligand system that can permeate into the affected tissues and counter the overproduction of superoxide.

CC Formula Patents for Review

US Library of Medicine Abstract

Superoxide dismutases (SOD) are essential enzymes that eliminate superoxide radicals (O2-) and thus protect cells from damage induced by free radicals. The active O2- production and low SOD activity in cancer cells may render the malignant cells highly dependent on SOD for survival and sensitive to inhibition of SOD. Here, we report that certain estrogen derivatives selectively kill human leukemia cells but not normal lymphocytes.

superoxide dismutase

Using complementary DNA microarray and biochemical approaches, we identify SOD as a target of this drug action. We show that chemical modifications at the 2-carbon (2-OH, 2-OCH3) of the derivatives are essential for SOD inhibition and apoptosis induction. Inhibition of SOD causes accumulation of cellular O2- and leads to free-radical-mediated damage to mitochondrial membranes, the release of cytochrome c from mitochondria, and apoptosis of the cancer cells.

Our results indicate that targeting that enzyme may be a promising approach to the selective killing of cancer cells and that mechanism-based combinations of SOD inhibitors with free-radical-producing agents may have clinical applications.

Department of Experimental Therapeutics, The University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.

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