Melatonin administration prevents lipopolysaccharide-induced oxidative damage in phenobarbital-treated animals

The protective effect of melatonin on lipopolysaccharide (LPS)-induced oxidative damage in phenobarbital-treated rats was measured using the following parameters: changes in total glutathione (tGSH) concentration, levels of oxidized glutathione (GSSG), the activity of the antioxidant enzyme glutathione peroxidase (GSH-PX) in both brain and liver, and the content of cytochrome P450 reductase in liver. Melatonin was injected intraperitoneally (ip, 4mg/kg BW) every hour for 4 h after LPS administration; control animals received 4 injections of diluent. LPS was given (ip, 4 mg/kg) 6 h before the animals were killed. Prior to the LPS injection, animals were pretreated with phenobarbital (PB), a stimulator of cytochrome P450 reductase, at a dose 80 mg/kg BW ip for 3 consecutive days. One group of animals received LPS together with N^w-nitro-L-arginine methyl ester (L-NAME), a blocker of nitric oxide synthase (NOS) (for 4 days given in drinking water at a concentration of 50 mM). In liver, PB, in all groups, increased significantly both the concentration of tGSH and the activity of GSH-PX. When the animals were injected with LPS the levels of tGSH and GSSG were significantly higher compared with other groups while melatonin and L-NAME significantly enhanced tGSH when compared with that in the LPS-treated rats. Melatonin alone reduced GSSG levels and enhanced the activity of GSH-PX in LPS-treated animals. Additionally, LPS diminished the content of cytochrome P450 reductase with this effect being largely prevented by L-NAME administration. Melatonin did not change the content of P450 either in PB- or LPS-treated animals. In brain, melatonin and L-NAME increased both tGSH levels and the activity of GSH-PX in LPS-treated animals. The results suggest that melatonin protects against LPS-induced oxidative toxicity in PB-treated animals in both liver and brain, and the findings are consistent with previously published observations related to the antioxidant activity of the pineal hormone.     

内皮衍生舒张因子对缺血（缺氧）,再灌注（复氧）心肌的保护作用

血管内皮产生的内皮衍生舒张因子（ｅｎｄｏｔｈｅｌｉｕｍ－ｄｅｒｉｖｅｄ ｒｅｌａｘｉｎｇ ｆａｃｔｏｒ,ＥＤＲＦ）即一氧化氮（ｎｉｔｒｉｃ ｏｘｉｄｅ,ＮＯ）本工作分别在大鼠Ｌａｎｇｅｎｄｏｒｆｆ离体心脏灌流模型和培养的大鼠心肌细胞上观察了ＮＯ、ＮＯ的前体物质Ｌ－精氨酸（Ｌ－Ａｒｇ）、ＮＯ的前体物质Ｌ－精氨酸（Ｌ－Ａｒｇ）、ＮＯ的合成阻断剂Ｌ－硝基精氨酸（Ｌ－ＮＮＡ）对心肌缺血（缺氧）再灌注（复氧     

心肌缺氧对大鼠心肌细胞内游离钙浓度的作用

本实验用ｆｕｒａ－２ 荧光技术研究离体鼠心缺氧期间心肌细胞内游离钙浓度（Ｃａ＾２＋）增加的机制。实验结果为：（１）Ｋｒｅｂｓ－Ｈｅｎｓｅｌｅｉｔ（Ｋ－Ｈ）液缺氧灌流离体鼠心脏引起（Ｃａ＾２＋）先慢后快地增国（２）无钙液氧灌流,仍能引起（Ｃａ蓿玻黾印＃ǎ常┖ǎǎ保薄粒保埃蓿担恚铮欤蹋┑模耍纫喝毖豕嗔鳎ǎ茫幔蓿玻┑谋浠嗨莆薷埔喝毖豕嗔鳎伊秸咭鸬模ǎ茫幔蓿玻┰黾樱飨缘陀?     

Calcium fluxes at plasmalemma and tonoplast

Abstract. An account is given of the characterization of calcium fluxes across plasmalemma and tonoplast membranes of root cortical cells, using compartmental analysis. Some of the assumptions associated with the method are discussed. Recent evidence regarding the concentration of free Ca²⁺ in plant cells, and the mechanisms driving active calcium transport across cell membranes, is reviewed. It is proposed that the evidence from whole cell studies and work at the molecular level is mutually supportive, and some speculation is ventured about the general pattern of calcium transport in higher plant cells.     

Phase behavior of isolated photoreceptor membrane lipids is modulated by bivalent cations

The phase behavior of isolated photoreceptor membrane lipids is further investigated by ³¹P-NMR, in view of earlier discrepant results [(1979) Biochim. Biophys. Acta 558, 330–337; (1982) FEBS Lett. 124, 93–99]. We present evidence that the discrepancy is due to bivalent cations. When resuspended in aqueous media at neutral pH in the absence of bivalent cations, the isolated photoreceptor membrane lipids largely adopt the bilayer configuration. However, upon addition of such cations (Ca²⁺ Mg²⁺) or when resuspended in their presence, the formation of other phases (hexagonal H_II, lipidic particles) results. The rate of this transition depends on cation concentration and temperature. The transition is not easily reversed by addition of EDTA. Implications with regard to photoreceptor membrane structure and function need further study.     

METABOLIC SEGREGATION OF INTRACELLULAR FREE AMINO ACIDS IN PLATYMONAS (CHLOROPHYTA)1

¹⁴C-amino acids were supplied to Platymonas subcordiformis (Wille) Hazen and the incorporation of radioactivity into protein and other compounds was followed. Alanine was rapidly metabolized by both N-limited and N-sufficient cells. Arginine and lysine were metabolized rapidly by N-limited cells, but were sequestered from metabolism in N-sufficient cells. This suggests the existence of two functionally distinct pools; a “metabolic” pool that is rapidly metabolized and preferentially used for incorporation into protein, and a “storage” pool rich in basic amino acids that is sequestered from metabolism.     

Changes occurring during aging and senescence in a submerged aquatic angiosperm (Potamogeton pectinatus)

Changes occurring during aging and senescence of leaves of a submerged aquatic angiosperm ( Potamogeton pectinatus L.) were studied. Total chlorophyll and chlorophylls a and b were maximal in mature, and minimal in old leaves. The chlorophyll a to b ratio was highest in mature leaves. During senescence, the chlorophyll content and the ratio of chlorophyll a to b decreased. The content of DNA, RNA, protein and dry weight, and the activity of alkaline pyrophosphatase decreased while free amino acids, the activity of protease, RNase and acid pyrophosphatase, and the ratio of acid to alkaline pyrophosphatase activity increased during aging and senescence. Kinetin (0.23 m M ) deferred leaf senescence by delaying the loss of chlorophyll, protein, nucleic acids and dry weight, and reducing the rise in free amino acids, the activity of protease, RNase and acid pyrophosphatase and the ratio of acid to alkaline pyrophosphatase activity; while both 0.69 m M ethrel and 0.075 m M ABA hastened senescence. Kinetin pretreatment for an optimum period (12 h) followed by ethrel or ABA treatment partially erased the senescence-promoting effect of the latter. But treatments in a reverse order markedly reduced the delaying effect of kinetin on senescence.     

Circadian placebo and ACTH effects on urinary cortisol in arthritics

The effect of placebo and ACTH-1-17 (Synchrodyn®, Hoechst) upon urinary free cortisol was examined at 5 different circadian stages on 10 men with Steinbrocker Stage II–III rheumatoid arthritis. A mean cosinor analysis of urinary cortisol data from the subjects prior to treatment with either ACTH or placebo revealed a statistically highly-significant rhythm. A circadian variation in a response of urinary free cortisol to a placebo was also seen. Moreover, the response of the midline-estimating statistic of rhythm (rhythm-adjusted circadian average) of urinary free cortisol to ACTH-1-17 by patients with rheumatoid arthritis is circadian rhythmic. This reactivity rhythm is out of phase with the spontaneous rhythm in urinary cortisol acrophases—in the tests limited thus far to midsummer. The further assessment of the circadian component in the context of broader interactions by rhythms with other frequencies in various conditions in health and disease is warranted by the demonstration of rhythms here presented for men with rheumatoid arthritis.     

Intracellular distribution and origin of sterols in Calendula officinalis leaves

In Calendula officinalis leaves 66% of all steryl forms are present in the ‘microsomal fraction’ (IV), 24% in the mitochondrial and Golgi membranes (III), 5% in the ‘chloroplast’ (II), 4% in the ‘cell wall and membrane’ (I) fraction and 1%. in the cytosol. Free sterols, their esters, glycosides and acylated glycosides are present in varying proportions in all cellular subtractions. Mevalonate-[2¹⁴C] labelling of sterols derived from various steryl forms showed that free sterols and all their derivatives, i.e. steryl esters and glucosides, are formed in fraction IV and are then translocated to other organelles. Fraction III is the main site of glycosylation of transported sterols as well as of acylation of steryl glycosides.