Role of antioxidants in the regulation of lipid peroxidation of preserved tissues during prolonged storage

The effect of natural and artificial antioxidant on accumulation of lipid peroxidation (LPO) products in preserved tissues during prolonged storage was studied. At the end of the characteristic period for each method of preservation the intensity of LPO was shown to switch from a low level to a self-accelerating regime. When antioxidants were used this critical transition appeared much later. Of the antioxidants, tested, vitamin E and propyl gallate were the most effective.Laboratory of Biophysics of Reception. A. I. Karaev Institute of Physiology, Academy of Sciences of the Azerbaijan SSr, Baku. (Presented by Academician of the Academy of Medical Sciences of the USSR G. G. Gasanov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 89, pp. 21–23, January, 1980.     

Melatonin and vitamin E limit nitric oxide-induced lipid peroxidation in rat brain homogenates

We have investigated the level of lipid peroxidation (LPO) in rat brain homogenates in the presence of nitric oxide (NO) which was released by the addition of sodium nitroprusside (SNP) and compared it with that induced by H₂O₂. We also examined the effect of melatonin and vitamin E on the NO-induced LPO. The concentration of malonaldehyde (MDA) plus 4-hydroxyalkenals (4-HDA) was used as an index of LPO. While both H₂O₂ and SNP increased MDA+4-HDA production in brain homogenates in a concentration-dependent manner, SNP was more potent than H₂O₂ at all concentrations tested. Both melatonin or vitamin E reduced NO-induced LPO in a dose-dependent manner in concentrations ranging from 10 μM to 10 mM. Under the in vitro conditions of this experiment, vitamin E was more efficient than melatonin in limiting NO-induced LPO in rat brain homogenates.     

Adverse effects of retinoic acid on embryo development and the selective expression of retinoic acid receptors in mouse blastocysts

BACKGROUND: All-trans retinoic acid (RA), the oxidative metabolite of vitamin A, is essential for normal development. In addition, high levels of RA are teratogenic in many species. We have previously shown that excess RA results in immediate effects on the preimplantation embryo and on blastocyst development. This study was conducted to clarify the long-term survival of mouse blastocyst and the effect of RA on gene expression. METHODS AND RESULTS: Using an in vitro model, we identified the immediate adverse impact of RA on mouse blastocyst development. This involved an inhibition of cell proliferation and growth retardation. Using an in vivo model, we also identified the resorption of postimplanted blastocysts that had been treated with excess RA. Analysis of RA-mediated gene induction was also included. The retinoic acid receptors RARalpha and RARgamma were constitutively expressed in the blastocyst and the inner cell mass, whereas RARbeta was induced upon RA treatment. CONCLUSIONS: This is the first evidence to show the impacts of RA on mouse blastocysts in vitro and any carry-over effects in the uterus. There is a retardation of early postimplantation blastocyst development and then subsequent blastocyst death. Our findings also show that there is some degree of selective induction of retinoic acid receptors when excess RA is administered to the blastocysts.