The reaction between allicin (diallylthiosulfinate), the active component of garlic and reduced glutathione was investigated. The product of this reaction, mixed disulfide S-allylmercaptoglutathione (GSSA) was separated by high performance liquid chromatography and identified by 1H and (13)C nuclear magnetic resonance and mass spectroscopy. The reaction is fast (with an apparent bimolecular reaction rate constant of 3.0 M(-1) s(-1)). It is pH-dependent, which reveals a direct correlation to the actual concentration of mercaptide ion (GS(-)). Both GSSA and S-allylmercaptocysteine (prepared from allicin and cysteine) reacted with SH-containing enzymes, papain and alcohol dehydrogenase from Thermoanaerobium brockii yielding the corresponding S-allylmercapto proteins, and caused inactivation of the enzymes. The activity was restored with dithiothreitol or 2-mercaptoethanol. In addition, GSSA also exhibited high antioxidant properties. It showed significant inhibition of the reaction between OH radicals and the spin trap 5,5'-dimethyl-1-pyroline N-oxide in the Fenton system as well as in the UV photolysis of H2O2. In ex vivo experiments done with fetal brain slices under iron-induced oxidative stress, GSSA significantly lowered the production levels of lipid peroxides. The similar activity of GSSA and allicin as SH-modifiers and antioxidants suggests that the thioallyl moiety has a key role in the biological activity of allicin and its derivatives.
Studies were conducted on the prenatal rat produce major disturbances in cell function, including given a single intraamniotic injection of ethyl docosahex-DNA fragmentation, damage to membrane ion transaenoate (Et-DHA; 9.6-12 mmol per fetus) or subjected porters and other proteins with rises in intracellular to an n-3 fatty acid-deficient diet to assess the role of Ca 2concentrations, and peroxidation of lipids (Hallidocosahexaenoate on oxidative stress during episodes well and Chirico, 1993). Evidence has accumulated to of ischemia. A time-dependent decrease in the ability of brain slices from animals treated with Et-DHA to produce suggest a causal relationship between oxidative stress thiobarbituric acid-reactive substance (TBARS), most and neurodegenerative disorders (Coyle and Puttfarpronounced after 1 day (from 58.1 ± 4.22 to 15.9 ± 1.6 cken, 1993). Brain trauma is linked to generation of nmol/mg of DNA), was noticed on stimulation with Fe2~.reactive oxygen species and production of lipid peroxBrain slices from fetuses treated for 1 day with Et-DHA ides (LPOs); furthermore, there are indications that and those from untreated fetuses produced TBARS levels oxygen radical formation and LPO are involved in of 46.7 ± 6.5 and 114.8 ± 10.8 nmol/mg of DNA, respecpathophysiological processes such as hypoperfusion, tively, after a 20-mm occlusion of the fetal-maternal ciredema, and axonal conduction failure (Hall and Braughculation at embryonic day 20, suggesting a protective ler, 1989). At the biochemical level, reactive oxygen effect of Et-DHA. The protective effeôt of a single dose species appear to alter NMDA receptor (Goel et al., of Et-DHA in utero remained high upto 3 days after injec-1993) and synaptosomal membrane (Viani et al., tion (p < 0.001) and was long-lasting, yet not significant, up to 3 days following birth. In agreement with a reduction 1995) functions, whereas oxygen radical scavengers in TBARS production by slices, the endogenous levels of can block posttraumatic consequences and promote TBARS in brains of Et-DHA-treated animals were lower functional recovery and survival in experimental anithan in the controls. Et-DHA-injected fetuses exhibited mals (Hall and Braughler, 1993). significantly higher levels of esterified DHA than the nonBrain tissue is particularly vulnerable to oxidative injected controls. n-3-deficient diet given to dams for 2 damage for several reasons, as recently discussed (Halweeks before birth did not affect the levels of TBARS liwell, 1992). Of these, the high content of polyunsatuproduction in control fetal brain slices but abolished the rated fatty acids (PUFAs), which are especially sensiincrease caused by ischemia. Et-DHA administration for tive to free radical attack, deserves attention. Being a 24 h to n-3-deficient fetuses reduced the amount of IBARS produced by the fetal brain slices from 49.1 major PUFA, docosahexaenoate (DHA) has the poten-± 8.5 to 31.7 ± 4.1 nmol/mg of DNA. A protective effect tial to increase the susceptibility of the membranes to fro...
Information on the prenatal accumulation of rat brain membrane lipids is scarce. In this study we investigated in detail the fatty acid (FA) composition of the rat brain, on each day from embryonic day 12 (E12) up to birth, and on 8 time points during the first 16 days of postnatal life, and correlated the FA changes with welldescribed events of neurogenesis and synaptogenesis. Between E14 and E17, there was a steep increase in the concentration of all the FAs: 16:0 increased by 136%, 18:0 by 139%, 18:1 by 92%, 20:4n-6 by 98%, 22:4n-6 by 116%, 22:5n-6 by 220%, and 22:6n-3 by 98%. After this period and up to birth, the concentration of the FAs plateaued, except that of 22:6n-3, which accumulated further, reaching an additional increase of 75%. After birth, except 22:5n-6, all FAs steadily increased at various rates. Estimation of the FA/PL molar ratios showed that prenatally the ratios of all the FAs either decreased or remained constant, but that of 22:6n-3 increased more than 2-fold; postnatally the ratios remained constant, with the exception of 22:4n-6 and 22:5n-6, which decreased.In conclusion, prenatal accumulation of brain fatty acids parallels important events in neurogenesis. 22:6n-3 is exceptional inasmuch in its steep accumulation occurs just prior to synaptogenesis. -Green, P., S. Glozman, B. Kamensky, and E. Yavin. Developmental chantes in rat brain membrane lipids and fatty acids: the preferential prenatal accumulation of docosahexaenoic acid.
Docosahexaenoic acid (DHA; 22:6n-3) is the major polyunsaturated fatty acid (FA) in the adult rat brain and it accumulates significantly more than any other FA prior to birth. Under normal nutritional conditions, fetal-brain DHA accumulation is substantial, with a "DHA accretion spurt" being demonstrated in the last period of gestation. Under stress conditions, this spurt may be harmful owing to an increase in multiple double-bond targets for lipid peroxidation. The "DHA accretion spurt" is supported by the maternal supply of DHA or its precursor. Under maternal dietary n-3 FA deficiency, DHA content in the fetal brain can be restored by direct intraamniotic injection of mM concentrations of ethyl-DHA (Et-DHA). This approach may hold a potential advantage in the event of maternal-fetal insufficiency, a stress that may cause intrauterine growth retardation. It also revealed a potential beneficial effect after in utero ischemic stress; brain slices from Et-DHA-treated fetuses formed less oxidation products, as detected by thiobarbituric acid (TBA), compared to controls. Furthermore, brain-lipid extracts from Et-DHA but not ethyl-oleate treated fetuses, exhibited hydroxyl radical scavenging activity, as demonstrated by electron spin-resonance technique. Part of the beneficial effect of Et-DHA administration on the fetal brain may be attributed to enhanced free-radical scavenging capability, a phenomenon not directly related to vitamin E or lipid-soluble antioxidant levels.
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