University at Buffalo (UB)
Release Date: June 11, 1995 This content is archived.
ATLANTA -- Researchers from the University at Buffalo are the first to show that the sperm of diabetic men sustain significant DNA damage due to free-radical oxidation.
Oxidative damage was found to be three to nine times greater in diabetic men than in healthy men. Damage to DNA of spermatozoa can contribute to congenital abnormalities in offspring.
Results of the research were presented here today at the annual meeting of the American Diabetes Association.
Scientist have known for some time that persons with diabetes are at risk for developing heart disease, blindness, premature aging and other degenerative diseases, and have speculated that this degeneration is caused in part by damage to cells from free radicals.
Free radicals -- compounds within cells than have an unpaired electron -- are by-products of normal metabolism. Their unpaired electron makes them extremely unstable, capable of bombarding and damaging surrounding cells. The existence of free radicals in human cells has been linked to the development of many health problems, including diabetes.
UB researchers led by Paresh Dandona, M.D., professor of medicine and a specialist in biological endocrinology, were the first to demonstrate increased DNA damage to white blood cells of diabetic men caused by free-radical oxidation. They now report similar damage to sperm.
The researchers collected sperm from nine patients with insulin-dependent diabetes mellitus and from 15 healthy males, and assessed the samples for markers of oxidative damage. They measured the concentrations of 8-hydroxy deoxyguanosine, or 8-OHdG -- an index of oxidative damage to DNA -- in spermatozoa, and the amount of lipid peroxidation, another indication of oxidative break-down, in seminal plasma.
Results showed that the 8-OHdG content indicates DNA oxidative damage was three to nine time greater in the sperm from diabetic men than in sperm of normal men.
Lipid peroxidation also was found to be significantly higher in seminal plasma of diabetics than in healthy controls.
Dandona said these findings need to be investigated further to determine if this damage to DNA could contribute to congenital abnormalities in babies fathered by diabetic men.
Members of the research team were Kuldip Thusu and Ahmad Aljada, doctoral candidates working with Dandona at Millard Fillmore Hospital, where he is chief of endocrinology; Thomas Nicotera, Ph.D., of Roswell Park Cancer Institute, and John Makowski, medical technologist.