A study by Zhanxiang Zhou, PhD, co-director of the UNC Greensboro Center for Translational Biomedical Research, found evidence of a pharmacological approach that in animal models reversed some of the effects of alcoholic liver disease.
It’s sweet. It’s bitter. It’s tangy and even tart. The tastes and types of alcohol seem endless. Despite the variety, alcohol when metabolized becomes one thing: toxic.
Through processes in the liver, alcohol is converted into a toxic metabolite called acetaldehyde. Acetaldehyde and its by-products contribute, particularly in chronic alcohol users, to the development of alcoholic liver disease (ALD). ALD is a leading cause of liver damage. It starts with steatosis or inflammation and can progress to hepatitis, cirrhosis and eventually liver cancer. Despite the prevalence, there is not an approved US Food and Drug Administration treatment.
Research by Zhanxiang Zhou, PhD, co-director of the UNC Greensboro Center for Translational Biomedical Research at the NC Research Campus in Kannapolis, NC, provided evidence of a pharmacological approach that in animal models reversed some of the effects of ALD. The findings were published in the Journal of Hepatology in the scientific paper “Pharmacological activation of aldehyde dehydrogenase 2 by Alda-1 reverses alcohol-induced hepatic steatosis and cell death in mice.”
Zhou, an expert in the study of liver disease, demonstrated the potential of the chemical compound Alda-1, an aldehyde dehydrogenase 2 (ALDH2) activator, to prompt the enzyme aldehyde dehydrogenase to break down acetaldehyde and its by-products faster and clear the toxins from the body more quickly.
The editors of the Journal of Hepatology noted that Zhou’s approach warrants further study because it illustrated effectively that “enhancing the ALDH2 activity by the use of Alda-1 can ameliorate several deleterious effects related to aldehydes and may provide a better protection against both acute and chronic injury pre-established by chronic alcohol exposure.”
“We established liver damage in our mouse model then we treated them with the Alda-1 compound for two weeks. We saw the reversal effect quite clearly,” said Zhou, whose previous research demonstrated that niacin and zinc supplementation mitigated the effects of alcohol-induced fatty liver disease.
He added, “I think the nutritional factors are good for protection of the liver and prevention of liver damage. For therapeutic applications, I think the pharmacological approach will prove to be best.”
With further study, Alda-1 may also prove effective as a treatment for people with a genetic polymorphism that inhibits ALDH2 function. In fact, eight percent of the world’s population including larger numbers of people of Asian descent are at higher risk for ALD due to this genetic mutation.
Zhou’s research with Alda-1 is still underway. “We are continuing the project to see if this compound can be used to treat other organ damage,” he said. “We want to see specifically whether Alda-1 can reduce the alcohol concentration in the brain.”
Learn more about UNC Greensboro’s Center for Translational Biomedical Research.