PubMed Health⌕ Search

Biomedical subjects

A Struck

Publications and source records attributed to A Struck.

9 recordsLinked to original sources
PubMed2001

Design, synthesis and properties of synthetic chlorophyll proteins.

A chemoselective method is described for coupling chlorophyll derivatives with an aldehyde group to synthetic peptides or proteins modified with an aminoxyacetyl group at the epsilon-amino group of a lysine residue. Three template-assembled antiparallel four-helix bundles were synthesized for the ligation of one or two chlorophylls. This was achieved by coupling unprotected peptides to cysteine residues of a cyclic decapeptide by thioether formation. The amphiphilic helices were designed to form a hydrophobic pocket for the chlorophyll derivatives. Chlorophyll derivatives Zn-methyl-pheophorbide b and Zn-methyl-pyropheophorbide d were used. The aldehyde group of these chlorophyll derivatives was ligated to the modified lysine group to form an oxime bond. The peptide-chlorophyll conjugates were characterized by electrospray mass spectrometry, analytical HPLC, and UV/visible spectroscopy. Two four-helix bundle chlorophyll conjugates were further characterized by size-exclusion chromatography, circular dichroism, and resonance Raman spectroscopy.

Amino Acid Sequence↗
PubMed1995

Inhibition of macrophage-dependent low density lipoprotein oxidation by nitric-oxide donors.

We have previously shown that nitric oxide donors inhibit the oxidation of low density lipoprotein (LDL) initiated by copper ions or by azo-bis-amidinopropane (Hogg et al., 1993. FEBS Lett. 334: 170-174). In this study, the nitric oxide donors S-nitroso-N-acetylpenicillamine (SNAP), spermine NONOate, and sodium nitroprusside were tested for their ability to inhibit macrophage-dependent oxidation of LDL. SNAP and spermine NONOate inhibited macrophage-dependent oxidation of LDL in a time- and concentration-dependent manner. We propose that nitric oxide is acting as a chain-breaking antioxidant that can inhibit the progression of lipid peroxidation in cell dependent-oxidation of LDL. By this mechanism nitric oxide could be an endogenous defense against atherogenesis. In contrast, sodium nitroprusside enhanced cell-mediated oxidation of LDL by a mechanism dependent on superoxide production and transition metal ions. Sodium nitroprusside also enhanced LDL oxidation by cell culture medium alone by a similar mechanism. The use of sodium nitroprusside as a nitric oxide donor in cellular systems appears to be complicated by the release of iron leading to an enhanced oxidative stress. Thus the effects of sodium nitroprusside in such systems may be unrelated to nitric oxide release.

Animals↗
PubMed1995

Role of apolipoprotein B-derived radical and alpha-tocopheroxyl radical in peroxidase-dependent oxidation of low density lipoprotein.

The peroxidation of low density lipoprotein (LDL) may play an important role in the modification of the lipoprotein to an atherogenic form. The oxidation of LDL by peroxidases has recently been suggested as a model for in vivo transition metal ion-independent oxidation of LDL (Wieland, E., S. Parthasarathy, and D. Steinberg. 1993. Proc. Natl. Acad. Sci. USA. 90: 5929-5933). It is possible that in vivo the peroxidase activities of proteins, such as prostaglandin synthase and myeloperoxidase, promote LDL oxidation. We have used horseradish peroxidase (HRP) and H2O2 as a model of peroxidase-dependent oxidation of LDL and we observed the following during HRP/H2O2-initiated LDL oxidation. i) The oxidation of alpha-tocopherol occurred with the concomitant formation of alpha-tocopheroxyl radical. This was followed by the production of an apolipoprotein B (apoB)-derived radical. The apoB radical and the alpha-tocopheroxyl radical were formed under both aerobic and anaerobic conditions. ii) Inclusion of N-t-butyl-alpha-phenylnitrone (PBN) did not inhibit alpha-tocopheroxyl radical formation. The ESR spectrum of a PBN/LDL-lipid derived adduct was observed after prolonged incubation. iii) There was formation of conjugated dienes, lipid hydroperoxides and thiobarbituric acid reactive substances. Our data indicate that HRP/H2O2 oxidizes both alpha-tocopherol and apoB to the corresponding radicals and concomitantly initiates lipid peroxidation.

Apolipoproteins B↗
PubMed1993

Inhibition of low-density lipoprotein oxidation by nitric oxide. Potential role in atherogenesis.

The effects of nitric oxide (.NO) and nitrovasodilators on the oxidation of low-density lipoprotein (LDL) have been studied. S-Nitroso-N-acetylpenicillamine (SNAP) and sodium nitroprusside (SNP) inhibited Cu(2+)- and 2,2'-azobis-2-amidinopropane hydrochloride-dependent oxidation of LDL as monitored by oxygen consumption and the formation of thiobarbituric acid-reactive substances, conjugated dienes, and lipid hydroperoxides. In the case of SNP, inhibition of LDL oxidation occurred only when the incubation mixture was irradiated with visible light. SNAP, however, exerted a dose-dependent inhibition of Cu(2+)-catalyzed oxidation of LDL even in the dark. Addition of .NO dissolved in deoxygenated buffer also inhibited the progression of LDL oxidation. Mouse peritoneal macrophages were less able to degrade LDL that had been oxidized in the presence of SNAP. Using an .NO electrode, it was estimated that a continuous production of .NO (< or = 760 nM/min) could retard the progression of LDL oxidation. We propose that .NO can inhibit LDL oxidation by acting as a chain-breaking antioxidant that is capable of scavenging carbon-centered and peroxyl radicals. Biological implications of this novel .NO antioxidant property are discussed in relation to atherogenesis and contrasted to the prooxidant property of .NO when generated in the presence of superoxide.

Animals↗
PubMed1992

Primary electron transfer kinetics in bacterial reaction centers with modified bacteriochlorophylls at the monomeric sites BA,B.

The primary electron transfer has been investigated by femtosecond time-resolved absorption spectroscopy in two chemically modified reaction centers (RC) of Rhodobacter sphaeroides, in which the monomeric bacteriochlorophylls BA and BB have both been exchanged by 13(2)-hydroxybacteriochlorophyll a or [3-vinyl]-13(2)-hydroxybacteriochlorophyll a. The kinetics of the primary electron transfer are not influenced by the 13(2)-hydroxy modification. In RCs containing [3-vinyl]-13(2)-hydroxybacteriochlorophyll a the primary rate is reduced by a factor of 10.

Bacteriochlorophylls↗
PubMed1990

Modified reaction centers from Rhodobacter sphaeroides R26. 2: Bacteriochlorophylls with modified C-3 substituents at sites BA and BB.

Monomeric bacteriochlorophylls BA and BB in photosynthetic reaction centers from Rhodobacter sphaeroides R26 were exchanged with (13(2)-hydroxy-)bacteriochlorophylls containing a 3-vinyl- or 3-(alpha-hydroxyethyl)-substituent instead of the 3-acetyl group. The corresponding binding sites must be tolerant to the introduction of the polar residue at C-13(2) and modifications of the 3-acetyl group. According to HPLC analysis, the exchange with both pigments amounts to less than or equal to 50% of the total BChl contained in the complex, corresponding to less than or equal to 100% of the monomeric BChl alpha BA,B. The absorption spectra show significant changes in the QX and QY-region of the monomeric bacteriochlorophylls. By contrast, the absorption of the primary donor (P870) and reversible photobleaching is retained. The circular dichroism is also unchanged in the 870 nm region. The positive cd band located at around 800 nm in native reaction centers, shifts with the (blue-shifted) QY absorption(s) of BA and/or BB, whereas the position of the negative one remains nearly unaffected. The data indicate that the latter is the upper excitonic band of the primary donor, and that there is little interaction of the monomeric BA/BB with the primary donor.

Bacteriochlorophylls↗
PubMed1990

Effects of n-3 fatty acids on renal function and renal prostaglandin E metabolism.

The present study was performed to investigate the effects of dietary fish oil supplements on renal function and renal prostaglandin (PG) E metabolism. The usual "western" diet of 10 healthy volunteers (six female and 4 male) aged between 21 and 35 years was supplemented with 6 g/day of n-3 polyunsaturated fatty acids [3.6 g of eicosapentaenoic acid (EPA) and 2.4 g of docosahexaenoic acid (DHA)] for six weeks. Supine arterial blood pressure (BP) and heart rate (HR), renal hemodynamics, renal excretory function and urinary excretion of PGE2 and PGE3 were determined before and at the end of the fish oil supplementation period. No changes could be observed in BP and HR while renal plasma flow (RPF), determined as the clearance of PAH, significantly increased from 559 +/- 44 to 738 +/- 47 ml/min (P less than 0.001) with the fish oil supplements. This was associated with a decrease in renal vascular resistance from (8.11 +/- 0.54).10(-2) to (6.37 +/- 0.38).10(-2) mm Hg.min.ml-1 (P less than 0.01). Glomerular filtration rate (GFR), determined as the clearance of inulin, increased from 97 +/- 3 to 107 +/- 3 ml/min (P less than 0.01), resulting in a decrease in filtration fraction from an average of 0.19 +/- 0.01 to 0.15 +/- 0.01 (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Fish oil and baroreceptor function in man.

The present study was designed to investigate the effects of dietary fish oil supplements on blood pressure, the pressor response to norepinephrine, and sensitivity of the arterial baroreceptor reflex. 10 normotensive volunteers (six female and 4 male) aged between 21 and 35 years were given 6 g/day of n-3 polyunsaturated fatty acids (3.6 g of eicosapentaenoic acid and 2.4 g of docosahexaenoic acid) during six weeks in addition to their usual diet. Resting blood pressure (BP), blood pressure response to exogenous norepinephrine (NE), and changes in heart rate (HR) associated with the blood pressure increase during NE infusion were determined before and at the end of the fish oil supplementation period. No changes in BP could be observed following the n-3 fatty acid supplements as compared to control values (110.7 +/- 2.4/63.5 +/- 2.9 mmHg vs. 110.6 +/- 1.9/60.1 +/- 1.3 mmHg). Blood pressure values during infusion of 0.1 micrograms/kg body weight of NE were 119.8 +/- 2.4/67.4 +/- 1.7 mmHg before the fish oil supplementation period and were also unchanged (119.9 +/- 2.0/70.5 +/- 1.9 mmHG) after the fish oil diet. HR during NE infusion was significantly (p less than 0.01) more suppressed after the fish oil supplementation period. During control, HR decreased in parallel with the rise in blood pressure from 69.2 +/- 2.8 min-1 to 63.9 +/- 2.4 min-1 (difference of 5.3 +/- 0.5 min-1), while after the fish oil supplementation HR fell from 68.1 +/- 3.5 min-1 to 56.2 +/- 2.6 min-1 (difference of 11.9 +/- 1.5 min-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗