cholecalciferol and Hypoxia-Ischemia--Brain

To investigate the concentration of vitamin D (VD), glutathione peroxidase (GP), superoxide dismutase (SOD), malondialdehyde (MDA), and advanced oxidation protein products (AOPP) in neonates with hypoxic-ischemic encephalopathy (HIE).. This study was performed prospectively in term neonates treated for HIE. Samples were collected from the neonates in study and control groups at 6-14 h and on day 5 of their lives for 25-OH vitamin D3, antioxidant enzymes including GP and SOD and oxidants substances including MDA and AOPP.. This study was performed with 31 term neonates with HIE and 30 healthy term neonates. Maternal VD level was statistically lower in the study group (9.8 ± 6.8 ng/mL) than the control (16.4 ± 8.7 ng/mL) (p = 0.002). SOD and MDA levels were significantly high, and VD level was significantly low in the study group on the first day of life (p = 0.001 and p = 0.028, respectively). SOD and GP levels were significantly high in the study group on day 5 (p < 0.05). VD was significantly low in the study group on day 5 and the proportion of subjects with VD below 5 ng/ml was significantly lower in the control group (p= <0.05).. VD has neuroprotective and antioxidant properties. We detected VD levels were low in infants with HIE and their mothers. This finding may be useful for decreasing of brain damage.

Topics: Adult; Advanced Oxidation Protein Products; Case-Control Studies; Cholecalciferol; Female; Glutathione Peroxidase; Humans; Hypoxia-Ischemia, Brain; Infant, Newborn; Male; Malondialdehyde; Prospective Studies; Superoxide Dismutase

Previous work in our laboratory has shown that long-term treatment with Vigconic 28 (VI-28), a Yang-invigorating Chinese herbal formula used for the promotion of overall wellness in Chinese medicine, can enhance the mitochondrial functional ability and antioxidant capacity in various tissues of both male and female rats. To investigate whether the VI-28 treatment regimen could afford tissue protection against oxidative injury, the effects of long-term VI-28 treatment (80 or 240 mg/kg/d x 30) on oxidative stress-induced tissue damage in various organs (brain, heart, liver, and kidney) were examined in female rats. The results indicated that long-term VI-28 treatment invariably protected against oxidative tissue damage in the rat models of cerebral/myocardial ischemia-reperfusion injury, CCl4 hepatotoxicity, and gentamicin nephrotoxicity. The tissue protection was associated with increases in the levels and activities of mitochondrial antioxidant components as well as with the preservation of mitochondrial structural integrity. This was evidenced by decreases in the sensitivity of mitochondria to Ca2+-induced permeability transition, and in the levels of mitochondrial malondialdehyde production, Ca2+ loading, and cytochrome c release in the tissues examined. Interestingly, the VI-28 treatment increased red cell CuZn-superoxide dismutase (CuZn-SOD) levels, and these levels correlated positively with the degree of tissue protection afforded by long-term VI-28 treatment in rats. The generalized tissue protection afforded by long-term VI-28 treatment may have clinical implications in the prevention of age-related diseases, and VI-28 treatment may possibly delay the aging process.

Topics: Animals; Carbon Tetrachloride; Carnosine; Chemical and Drug Induced Liver Injury; Cholecalciferol; Cytoprotection; DNA Damage; Drugs, Chinese Herbal; Female; Gentamicins; Hypoxia-Ischemia, Brain; Kidney Diseases; Liver Diseases; Male; Myocardial Reperfusion Injury; Oxidative Stress; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Superoxide Dismutase; Time Factors; Yang Deficiency