Evaluating the safety of energy drink, alcohol consumption
A study published in the Journal of Food Science examines the effects of energy drink (ED) exposure either alone or in combination with alcohol (ethanol) on oxidative stress parameters including superoxide dismutase, catalase, glutathione peroxidase, and lipid peroxidation parameter malondialdehyde in rats.
Over the past decade, energy drink consumption among young adults has increased, especially combined with alcoholic beverages. A study published in the Journal of Food Science examines the effects of energy drink (ED) exposure either alone or in combination with alcohol (ethanol) on oxidative stress parameters including superoxide dismutase, catalase, glutathione peroxidase, and lipid peroxidation parameter malondialdehyde in rats. Oxidative stress is attributed to the etiology of several diseases such as diabetes, cancer, and cardiovascular disorders.
The researchers divided 36 Sprague-Dawley rats into control and five treatment groups. The control group received tap water while the treatment groups received: low-dose ED, high-dose ED, ethanol, ethanol mixed with low-dose ED, and ethanol mixed with high-dose ED. They administered the treatments via oral gavage for 14 days. The dose of ED was designed based on the consumption of one container of ED (250 mL) per day by an adult weighing 65 kg (~143 lb) for low-dose ED and two containers (500 mL) per day for high-dose ED exposed group.
The researchers found that ED exposure led to a dose-dependent increase in liver lipid peroxidation parameter malondialdehyde (MDA) compared to the control, indicating oxidative damage. Histopathological findings also revealed that ED alone may generate liver damage. Ethanol exposure increased MDA level and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activity in both the brain and the liver. The combination of ethanol and ED produced greater damage, which is considered by further increases in SOD and GSH-Px activity in the brain. Similar results for MDA were observed in both the liver and brain as well.
The researchers concluded that ED consumption—especially in exaggerated amounts—might be a risk factor for antioxidative stress, as indicated by decreased brain SOD activity. Also, the particular combination of EDs’ ingredients may be responsible for the augmentation of oxidative stress parameters and histopathological abnormalities in liver and to some extent in brain tissue. Thus, consumption of EDs especially with alcoholic beverages appears to represent a significant public health concern due to the increased toxicological consequences both peripherally and centrally.