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Nitroxide radicals protect cultured rat embryos and yolk sacs from diabetic-induced damage
Seonghun Ryu1, Roni Kohen, Amram Samuni
1Laboratory of Teratology, Department of Anatomy and Cell Biology, Hebrew University-Hadassah Medical School, Jerusalem, Israel 91120.
Background:
Diabetic teratogenicity relates, partly, to embryonic oxidative stress and the extent of the embryonic damage can apparently be reduced by antioxidants. We investigated the effects of superoxide dismutase-mimics nitroxides, 2,2,6,6-tetramethyl piperidine-N-oxyl (TPL) as an effective antioxidant, on diabetes-induced embryopathy.
Methods:
Embryos (10.5 day old) and their yolk sacs from Sabra female rats were cultured for 28 h in the absence or in the presence of nitroxides at 0.05-0.4 mM in control, diabetic subteratogenic, or diabetic teratogenic media, and monitored for growth retardation and congenital anomalies. The oxidant/antioxidant status was examined by oxygen radical absorbance capacity and lipid peroxidation assays, whereas the yolk sac function was evaluated by endocytosis assay.
Results:
Diabetic culture medium inhibited embryonic and yolk sac growth, induced a high rate of NTDs, reduced yolk sac endocytosis and embryonic antioxidant capacity, and increased lipid peroxidation. These effects were more prominent in the embryos with NTD compared to those without NTD. TPL added to diabetic teratogenic medium improved embryonic and yolk sac growth, reduced the rate of NTDs, and improved yolk sac function. The oxidant/antioxidant status of embryos was also improved. TPL at 1 mM did not damage the embryos cultured in control medium.
Conclusions:
In diabetic culture medium, oxidative damage is higher in the malformed rat embryos compared to those without anomalies; the nitroxide provides protection against diabetes-induced teratogenicity in a dose-dependent manner. The yolk sac damage, apparently caused by the same mechanism, might be an additional contributor to the embryonic damage observed in diabetes.
Insights
Antioxidants like TPL can protect against diabetes-induced birth defects in embryos by reducing oxidative stress. This study shows TPL improves embryonic and yolk sac development in diabetic conditions.
Area of Science:
- Reproductive biology
- Developmental toxicology
- Biochemistry
Background:
- Diabetic embryopathy is linked to embryonic oxidative stress.
- Antioxidants show potential in mitigating diabetes-induced embryonic damage.
Purpose of the Study:
- To investigate the protective effects of superoxide dismutase-mimics nitroxides, specifically 2,2,6,6-tetramethyl piperidine-N-oxyl (TPL), against diabetes-induced embryopathy.
Main Methods:
- Rat embryos and yolk sacs were cultured in control, diabetic subteratogenic, or diabetic teratogenic media with varying concentrations of TPL.
- Assessed embryonic and yolk sac growth, congenital anomalies, oxidant/antioxidant status, and yolk sac endocytosis.
Main Results:
- Diabetic medium impaired embryonic/yolk sac growth, increased congenital anomalies, and reduced antioxidant capacity.
- TPL treatment improved growth, reduced anomalies, and restored antioxidant status in diabetic embryos.
- TPL did not harm embryos in control medium.
Conclusions:
- Oxidative damage is elevated in malformed diabetic rat embryos.
- TPL offers dose-dependent protection against diabetes-induced teratogenicity.
- Yolk sac damage may contribute to embryonic defects in diabetes.
