Resveratrol ameliorates DNA damage, prooxidant and antioxidant imbalance in 1,2-dimethylhydrazine induced rat colon carcinogenesis.

Research on trans-resveratrol has been picking up steam in recent years, leaving the world to wonder if there’s anything this incredible natural antioxidant can’t do. And amazingly, the news just keeps getting better.

In a new study, researchers examined the effects of trans-resveratrol on rats with colon cancer. The rats were divided into four groups according to treatment—one that received a chemical to induce cancer (called 1,2-dimethylhydrazine, or DHM for short), one that received DHM and trans-resveratrol, one that received only trans-resveratrol, and finally, one that received no treatment to serve as a control.

Over the course of this 30-week study, researchers had two major goals: to evaluate the short-term effect that this powerful compound would have on DNA damage and to evaluate the long-term effect it would have on membrane lipid peroxidation (the process by which free radicals cause damage to cell membranes). In addition, the researchers measured the levels of circulating antioxidants.

The results? Rats supplemented with trans-resveratrol showed significantly less white blood cell damage than those that received DHM alone. What’s more, those that received trans-resveratrol for the full 30 weeks also showed a marked increase in several key antioxidant enzymes—including superoxide dismutase, catalase and glutathione reductase—along with other antioxidant factors like vitamin C, vitamin E and beta-carotene. Finally, this group of rats also showed a noticeable decrease in markers of dangerous lipid peroxidation.1

In the end, the study authors’ conclusion couldn’t be more clear—or promising, for that matter—stating “results indicate that DMH-induced DNA damage and oxidative stress were suppressed/prevented effectively by chronic resveratrol supplementation.”

So does that mean getting your daily dose of trans-resveratrol can keep your colon safe? Without a human study, there’s no way to say for sure. But with all of the other proven benefits provided by trans-resveratrol, one thing is certain: adding it to your daily supplement program today is one of the smartest moves you can make.

Resveratrol ameliorates DNA damage, prooxidant and antioxidant imbalance in 1,2-dimethylhydrazine induced rat colon carcinogenesis.

Sengottuvelan M, Deeptha K, Nalini N.

Department of Biochemistry and Biotechnology, Annamalai University, Tamilnadu, India.

Colorectal cancer is one of the most common internal malignancies in Western society. Currently oxidative stress has been increasingly postulated as a major contributor to carcinogenesis. The assessment of damage in various biological matrices, such as tissues and cells, is vital to understand the development of carcinogenesis and subsequently devising intervention strategies. Thus, the major objective of the present study was to examine the effect of resveratrol (Res) on DNA damage in a short-term study of 16 days and circulatory lipid peroxidation, enzymic/non-enzymic antioxidants status in a long-term study of 30 weeks in 1,2-dimethylhydrazine (DMH) induced colon carcinogenesis. Wistar male rats were divided into 6 groups, group 1 were control rats, group 2 rats received Res (8mg/kg body weight, orally, everyday), rats in groups 3-6 were administered (DMH, 20mg/kg body weight, s.c.) as four injections in order to induce DNA damage in the short-term or once a week for the first 15 weeks in the long-term study. In addition to DMH, group 4 (initiation), 5 (post-initiation) and 6 (entire-period) received Res (8mg/kg body weight, p.o., everyday). The results revealed that, supplementation with Res (entire-period) treatment regimen significantly reduced the DMH-induced leukocytic DNA damage (tail length, tail moment, % DNA in the comet tail and olive tail moment) as compared to DMH-alone treated rats. In addition, entire-period Res supplementation increased the enzymic (superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase and glutathione S-transferase) and non-enzymic (reduced glutathione, vitamin C, vitamin E and beta-carotene) antioxidant status with a corresponding decrease in the extent of lipid peroxidation markers (thiobarbituric acid reactive substances, diene conjugates and lipid hydroperoxides). Conversely, Res supplementation during initiation and post-initiation regimen did not produce greater modulatory effects. Our results indicate that DMH-induced DNA damage and oxidative stress were suppressed/prevented effectively by chronic Res supplementation.