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1.
2.
H K Sharma H R Prasanna R S Lane M Rothstein 《Archives of biochemistry and biophysics》1979,194(1):275-282
The rates of synthesis and degradation of enolase and total soluble proteins slow with age in the free-living nematode, Turbatrix aceti. The half-lives are 73 and 58 h for soluble protein and enolase, respectively, in young organisms (5 days old). The respective figures are 163 and 161 h for old organisms (22–30 days old). Similar slowing of protein turnover occurs when the organisms are aged by a repeated screening procedure which avoids the use of fluorodeoxyuridine, an inhibitor of DNA synthesis normally added to aging cultures to obtain synchrony. The results support the idea that slowed protein turnover may be responsible for the formation of altered enzymes in old organisms. 相似文献
3.
Murthy S. D. S.; Sabat Surendra Chandra; Mohanty Prasanna 《Plant & cell physiology》1989,30(8):1153-1157
Addition of low concentrations of mercury chloride (HgCl2 tointact cells of the cyanobacterium, Spirulina platensis causedan enhancement in the intensity of fluorescence emitted fromphycocyanin at room temperature and induced blue shifts in theemission peak suggestive of changes in energy transfer withinthe phycobilisomes. HgCl2 also suppressed the whole-chain electrontransport activity (H2O methylviologen) at much lower concentrationsthan that required to inhibit Hill activity supported by para-benzoquinone.The extent of inhibition of Hill activity was much higher underhigh-intensity light than that under low-intensity light. Ourresults indicate that mercury ions at low concentrations affectthe transfer of energy within phycobilisomes and at high concentrationsthey inhibit electron transport in this cyanobacterium. (Received February 21, 1989; Accepted October 2, 1989) 相似文献
4.
H R Prasanna K D Nakamura S F Ali M H Lu W Slikker R W Hart 《Biochemical and biophysical research communications》1989,160(1):217-221
The microsomal activation of the potent hepatocarcinogen aflatoxin B1 (AFB1) and the expression of selected protooncogenes were investigated in the livers of rats exposed to delta 9-tetrahydrocannabinol (THC). At equimolar levels of cytochrome P-450, the microsome-mediated binding of AFB1 to DNA was significantly lower (56% of the controls) in preparations from drug exposed rats. Hepatic expression of the c-k-ras protooncogene was 3-fold higher in THC exposed animals. These results suggest the possible occurrence of long lasting residual effects in the rats exposed to THC. 相似文献
5.
Previous investigations in our laboratory demonstrated the existence of an intrinsic mechanism, termed membrane modulation, capable of restoring sensitivity to aspirin treated platelets, resulting in irreversible aggregation in response to arachidonic acid (AA). The mechanism underlying correction of aspirin induced inhibition of platelet function, however, was not clear. In the present study we have evaluated the role of lipoxygenase (LO) metabolites of AA in securing irreversible aggregation of drug induced cyclooxygenase (CO) deficient platelets. Platelets treated with aspirin or Ibuprofen did not convert radiolabeled AA to thromboxane, but generated significant quantities of hydroxy acids via the LO pathway. However, drug exposed platelets, when stirred with epinephrine first and then challenged with AA, aggregated irreversibly. Eicosatetraynoic acid (ETYA 1, U53119) inhibited AA conversion by the LO pathway, whereas 5,8,11,14-eicosatetraynoic acid (ETYA 2) inhibited AA conversion by both CO and LO enzymes. Yet, at the inhibitory concentration these fatty acids failed to prevent AA induced irreversible aggregation of CO deficient, alpha adrenergic receptor stimulated platelets. Results of four studies show that the generation of LO metabolites of AA are not essential for securing irreversible aggregation of platelets. 相似文献
6.
Δ2-Thiazoline-2-carboxylate, the product of the suspected physiological reaction catalyzed by
-amino acid oxidase, is stable to hydrolysis at 37°C and pH 7 or above, but it hydrolyzes readily at pH 5 or below to give a mixture of N- and S-oxalylcysteamines; the N-oxalyl derivative predominates at pH's above 1 while the S-oxyalyl compound is the major product at high acidities. The pH-rate profile looks like the superposition of two bell-shaped curves. The initial increase in the rate as the pH is lowered is controlled by a pKa of 3.95 and from pH 1 to 3 the rate is relatively constant (k = 6.7 × 10−4s−1 at 37°C and ionic strength 0.5
). Below pH 1 the rate increases again to a maximum in 1
HCl and then decreases in more highly acidic solutions. The rate of conversion of S-oxalylcysteamine to N-oxalylcysteamine is inversely proportional to the hydrogen ion concentration from pH 3 to 5 but becomes largely independent of pH from pH 1 to 2. In the pH-independent region the rate is comparable with that observed by others for S-acetylcysteamine but in the pH-dependent region the rate is 20 to 25 times faster for the oxalyl derivative than for the acetyl compound. At pH 1, N-oxalylcysteamine is partially converted to the S-oxalyl derivative but the rate of hydrolysis (k = 1.0 × 10−5s−1 at 37°C) to cysteamine and oxalate of this partially equilibrated system occurs at a comparable rate. The results of this investigation are rationalized in terms of what is known about other thiazoline hydrolyses and intramolecular S to N acyl migrations. The main differences in the present case are presumably due to the fact that thiazoline-2-carboxylate can undergo hydrolysis by two reaction manifolds, one with the carboxyl unprotonated and the other with it protonated. The relevance of these results to possible reactions of thiazoline-2-carboxylate in vivo is briefly considered. 相似文献
7.
Anusha Parthiban Selvamani Vijayalingam K. Radha Shanmugasundaram Rema Mohan 《Cell biology international》1995,19(12):987-994
Erythrocytes isolated from 131 cases of Non-Insulin Dependent Diabetes Mellitus (NIDDM) were studied for lipid peroxidation, antioxidant defences, and the maximum peroxidisable substrate in the cell membrane. Antioxidant defences are lowered in NIDDM, followed by significant rise in lipid peroxidation products. However, in the erythrocyte membrane, the total polyunsaturated peroxidisable lipids are lower than in normal erythrocytes which may be a causative factor affecting the survival of the cells. 相似文献
8.
The activity of alkaline phosphate and2+-Mg2+ adenosine triphosphatase, two of the enzymes involved in limpid and calcium uptake across the intestinal membrane, were increased
in experimental atherosclerosis. Administration ofAnnapavala sindhooram, an antiatherosclerotic drug, lowers these enzyme levels to near normal values. Prostaglandin E2 stimulated the enzyme activitiesin vitro, while prostaglandin endoperoxide inhibited the activity. Thromboxane and other prostaglandins had no effect on the enzyme
activities. Addition of the antiatherosclerotic drug to thein vitro assay system reversed the effect of both prostaglandin E2 and prostaglandin endoperoxide. 相似文献
9.
The dark-relaxation kinetics of variable fluorescence, Fv, in intact green leaves of Pisum stativum L. and Dolichos lablab L. were analyzed using modulated fluorometers. Fast (t1/2 = 1 s) and slow (t1/2 = 7–8 s) phases in fv dark-decay kinetics were observed; the rate and the relative contribution of each phase in total relaxation depended upon the fluence rate of the actinic light and the point in the induction curve at which the actinic light was switched off. The rate of the slow phase was accelerated markedly by illumination with far-red light; the slow phase was abolished by methyl viologen. The halftime of the fast phase of Fv dark decay decreased from 250 ms in dark-adapted leaves to 12–15 ms upon adaptation to red light which is absorbed by PSII. The analysis of the effect of far-red light, which is absorbed mainly by PSI, on Fv dark decay indicates that the slow phase develops when a fraction of QA
– (the primary stable electron acceptor of PSII) cannot transfer electrons to PSI because of limitation on the availability of P700+ (the primary electron donor of PSI). After prolonged illumination of dark-adapted leaves in red (PSII-absorbed) light, a transient. Fv rise appears which is prevented by far-red (PSI-absorbed) light. This transient fv rise reflects the accumulation of QA
– in the dark. The observation of this transient Fv rise even in the presence of the uncoupler carbonylcyanide m-chlorophenyl hydrazone (CCCP) indicates that a mechanism other than ATP-driven back-transfer of electrons to QA may be responsible for the phenomenon. It is suggested that the fast phase in Fv dark-decay kinetics represents the reoxidation of QA
– by the electron-transport chain to PSI, whereas the slow phase is likely to be related to the interaction of QA
– with the donor side of PSII.Abbreviations CCCP
carbonylcyanide m-chlorophenylhydrazone
- FO
initial fluorescence level
- Fv
variable fluorescence
- P700
primary electron donor of PSI
- PSI, II
photosystem I, II
- QA (QA
–) QB (QB
–)
primary and secondary stable electron acceptor of PSII in oxidized (reduced) state
Supported by grant B6.1/88 DST, Govt. of India. 相似文献
10.
Ni2+ inhibits electron-transport activity of isolated barley chloroplasts and this inhibition of electron transport by Ni2+ is distinctly different from other heavy metal ion (e.g., Pb2+, Cd2+, Zn2+)-induced inhibition of chloroplast function. Ni2+ inactivates Photosystem II (PS II) activity at a lower concentration than that required for the same extent of inhibition of Photosystem I (PS I)-mediated electron flow. Ni2+ induces changes in chlorophyll a (Chl a) emission characteristics and brings about a lowering of the Chl a fluorescence yield, and this lowering of Chl a fluorescence intensity is not relieved by the exogenously supplied electron donor NH2OH which donates electrons very close to the PS II reaction centres. Immobilization of the chloroplast membrane structure with glutaraldehyde fails to arrest the Ni2+-induced loss of PS II activity. Also, Ni2+-treated chloroplasts do not regain the ability to photoreduce 2,6-dichlorophenolindophenol even after washing of chloroplasts with buffer. These results indicate that unlike Zn2+ or Pb2+, Ni2+ induces alterations in the chloroplast photosynthetic apparatus resulting in an irreversible loss of electron-transport activity. 相似文献