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1.
Summary. Diabetes mellitus is a primary contributor to progressive kidney dysfunction leading to end-stage renal disease (ESRD). In
the early phase of diabetes, prior to the onset of further complications, both kidney size and glomerular filtration rate
(GFR) increase. Glomerular hyperfiltration is considered a risk factor for downstream complications and progression to ESRD.
Abnormalities in vascular control have been purported to account for the glomerular hyperfiltration in early diabetes. In
this review we discuss a tubulo-centric concept in which tubular growth and subsequent hyper-reabsorption contribute to the onset of glomerular hyperfiltration that
demarks the early stage of diabetes. Kidney growth, in this concept, is no longer relegated to a compensatory response to
hyperfiltration, but rather plays a primary and active role in its genesis and progression. As such, components of kidney growth, such as the polyamines, may provide a means of
early detection of diabetic kidney dysfunction and more effective therapeutic intervention. 相似文献
2.
I. B. Zavodnik I. K. Dremza E. A. Lapshina V. T. Cheshchevik 《Biochemistry (Moscow) Supplemental Series A: Membrane and Cell Biology》2011,5(2):101-110
Diabetes mellitus is a complex polygenic pathology, which is characterized by numerous metabolic disorders. Progressive hyperglycemia
developing during this disease causes clinically significant tissue damage and is considered as a main risk factor of micro-
and macrovascular complications leading to retinopathy, nephropathy, and neuropathy. Hyperglycemia-depended oxidative stress
and impairments in nitric oxide bioavailability play an essential role in the pathogenesis of diabetes and its complications.
Homeostasis of glucose maintained by metabolic effects of insulin includes an increase of glucose uptake by skeletal muscles
and suppression of glucose production by the liver. M. Brownlee (2005) put forward a hypothesis assuming that oxidative stress
is the main mechanism of diabetic tissue damages. According to this hypothesis, mitochondrial dysfunction and superoxide anion
radical hyperproduction by mitochondria is the principal mechanism of activation of four pathways of hyperglycemia-induced
impairments under diabetes. Two cell signaling cascades regulate the glucose homeostasis: insulin-mediated glucose uptake
(IMGU) in skeletal muscles, liver, and heart and glucose-stimulated insulin secretion (GSIS) in pancreatic β-cells. In addition
to nonspecific irreversible oxidative damage of DNA, protein and lipid molecules reactive oxygen and nitrogen species induce
cell and tissue damage, activating a number of cell stress-sensitive signaling cascades. Stress-dependent serine phosphorylation
of insulin receptor substrate (IRS) proteins decreases its capacity for tyrosine phosphorylation and may accelerate degradation
of IRS. This process underlies the molecular mechanism of oxidative stress-induced insulin resistance. 相似文献
3.
Summary. The pathogenesis of several neurodegenerative diseases, including Alzheimer’s disease, has been linked to a condition of oxidative
and nitrosative stress, arising from the imbalance between increased reactive oxygen species (ROS) and reactive nitrogen species
(RNS) production and antioxidant defences or efficiency of repair or removal systems. The effects of free radicals are expressed
by the accumulation of oxidative damage to biomolecules: nucleic acids, lipids and proteins. In this review we focused our
attention on the large body of evidence of oxidative damage to protein in Alzheimer’s disease brain and peripheral cells as
well as in their role in signalling pathways. The progress in the understanding of the molecular alterations underlying Alzheimer’s
disease will be useful in developing successful preventive and therapeutic strategies, since available drugs can only temporarily
stabilize the disease, but are not able to block the neurodegenerative process. 相似文献
4.
Protein-bound advanced glycation endproducts (AGEs) as bioactive amino acid derivatives in foods 总被引:2,自引:0,他引:2
Henle T 《Amino acids》2005,29(4):313-322
Summary. The Maillard reaction or nonenzymatic browning is of outstanding importance for the formation of flavour and colour of heated
foods. Corresponding reactions, also referred to as “glycation”, are known from biological systems, where the formation of
advanced glycation endproducts (AGEs) shall play an important pathophysiological role in diabetes and uremia. In this review,
pathways leading to the formation of individual protein-bound lysine and arginine derivatives in foods are described and nutritional
consequences resulting from this posttranslational modifications of food proteins are discussed. 相似文献
5.
Diabetic nephropathy: mechanisms of renal disease progression 总被引:5,自引:0,他引:5
Kanwar YS Wada J Sun L Xie P Wallner EI Chen S Chugh S Danesh FR 《Experimental biology and medicine (Maywood, N.J.)》2008,233(1):4-11
Diabetic nephropathy is characterized by excessive amassing of extracellular matrix (ECM) with thickening of glomerular and tubular basement membranes and increased amount of mesangial matrix, which ultimately progress to glomerulosclerosis and tubulo-interstitial fibrosis. In view of this outcome, it would mean that all the kidney cellular elements, i.e., glomerular endothelia, mesangial cells, podocytes, and tubular epithelia, are targets of hyperglycemic injury. Conceivably, high glucose activates various pathways via similar mechanisms in different cell types of the kidney except for minor exceptions that are related to the selective expression of a given molecule in a particular renal compartment. To begin with, there is an obligatory excessive channeling of glucose intermediaries into various metabolic pathways with generation of advanced glycation products (AGEs), activation of protein kinase C (PKC), increased expression of transforming growth factor-beta (TGF-beta), GTP-binding proteins, and generation of reactive oxygen species (ROS). The ROS seem to be the common denominator in various pathways and are central to the pathogenesis of hyperglycemic injury. In addition, there are marked alterations in intraglomerular hemodynamics, i.e., hyperfiltration, and this along with metabolic derangements adversely compounds the hyperglycemia-induced injury. Here, the information compiled under various subtitles of this article is derived from an enormous amount of data summarized in several excellent literature reviews, and thus their further reading is suggested to gain in-depth knowledge of each of the subject matter. 相似文献
6.
The role of oxidative stress in diabetic complications 总被引:14,自引:0,他引:14
The morbidity and mortality associated with diabetes is the result of the myriad complications related to the disease. One
of the most explored hypotheses to explain the onset of complications is a hyperglycemia-induced increase in oxidative stress.
Reactive oxygen species (ROS) are produced by oxidative phosphorylation, nicotinamide adenine dinucleotide phosphate oxidase
(NADPH), xanthine oxidase, the uncoupling of lipoxygenases, cytochrome P450 monooxygenases, and glucose autoxidation. Once
formed, ROS deplete antioxidant defenses, rendering the affected cells and tissues more susceptible to oxidative damage. Lipid,
DNA, and protein are the cellular targets for oxidation, leading to changes in cellular structure and function. Recent evidence
suggests ROS are also important as second messengers in the regulation of intracellular signaling pathways and, ultimately,
gene expression. This review explores the production of ROS and the propagation and consequences of oxidative stress in diabetes. 相似文献
7.
Elevated glomerular filtration rate (GFR) is a frequent finding in patients with early insulin-dependent diabetes mellitus (IDDM). The mechanisms responsible for this glomerular hyperfiltration in IDDM are unclear. Rats made diabetic with alloxan or streptozotocin, and treated daily with supplemental insulin, have moderate hyperglycemia and elevated GFR, and thus have been used to study mechanisms of glomerular hyperfiltration in diabetes. Renal micropuncture techniques have shown that single-nephron GFR (SNGFR) is elevated in moderately hyperglycemic diabetic rats. In some cases, this is because of elevated glomerular capillary pressure (Pgc), but in other cases, Pgc is normal despite elevated SNGFR. Several potential mediators of increased SNGFR have been examined, including hyperglycemia, increased glomerular prostaglandin production, and decreased sensitivity of the tubuloglomerular feedback mechanism. Renal failure is a common complication of human IDDM. Diabetic rats with long-term moderate hyperglycemia have been used to study the mechanism by which glomerular injury develops in diabetes mellitus. It has been postulated that glomerular hyperfiltration or some determinant of elevated GFR in early diabetes may ultimately cause glomerular damage, leading to a progressive loss of renal function (diabetic nephropathy). Diabetic rats with long-term moderate hyperglycemia, however, do not develop characteristic glomerular lesions of human diabetic nephropathy and, in fact, develop only minimal glomerular injury even after 1 year of diabetes. Thus, although the diabetic rat with moderate hyperglycemia may be useful to study the mechanisms of glomerular hyperfiltration in early diabetes, it may not be an appropriate model of renal failure in IDDM. 相似文献
8.
Agostinelli E Tempera G Molinari A Salvi M Battaglia V Toninello A Arancia G 《Amino acids》2007,33(2):175-187
Summary. In tumours, polyamines and amine oxidases increase as compared to normal tissues. Cytotoxicity induced by bovine serum amine
oxidase (BSAO) and spermine is attributed to H2O2 and aldehydes produced by the reaction. Increasing the incubation temperature from 37 to 42 °C enhances cytotoxicity in cells
exposed to spermine metabolites. The combination BSAO/spermine prevents tumour growth, particularly well if the enzyme has
been conjugated with a biocompatible hydrogel polymer. Since the tumour cells release endogenous substrates of BSAO, the administration
of spermine is not required. Combination with hyperthermia improves the cytocidal effect of polyamines oxidation products.
Our findings show that multidrug resistant (MDR) cells are more sensitive to spermine metabolites than their wild-type counterparts,
due to an increased mitochondrial activity which induces the generation of intracellular ROS prior to the onset of mitochondrial
permeability transition (MPT). It makes this new approach attractive, since the development of MDR is one of the major problems
of conventional cancer therapy. 相似文献
9.
Summary. Glucocorticoid hormones enhance the reabsorptive capacity of filtered amino acids in rat kidney, as it was shown in previous
in vivo clearance experiments. In the present study, the site of glucocorticoid action on neutral amino acid transport in superficial
nephrons of rat kidney was investigated using in vivo micropuncture technique. Adult female Wistar rats were treated with dexamethasone (DEX), and fractional excretion of L-glutamine
(L-Gln) and L-leucine (L-Leu) were determined and related to inulin after microinfusion into different nephron segments. DEX
reduced fractional excretion of both neutral amino acids as a sign of enhanced reabsorptive capacity. The site of main DEX
action on L-Leu reabsorption has been localized in the proximal straight tubule. However, in the case of L-Gln, the inhibition
of γ-glutamyltranspeptidase (γ-GT) by administration of acivicin indicated the importance of this brush border enzyme in reduced L-Gln excretion. DEX enhanced
γ-GT activity by tubular acidification. It can be presumed a DEX-inducible transport system for neutral amino acids mainly
localized in proximal straight tubules of rat kidney.
Received July 8, 1999 相似文献
10.
Summary. Glutamine is one of the most abundant free amino acid found in raw food. In this study, the contribution of free glutamine
to nonenzymatic browning and fluorescence was investigated using an aqueous model system with methylglyoxal. The results indicated
that glutamine contributed to the Maillard reaction via two pathways. First, the hydrolysis of the amide bond of glutamine
led to the release of ammonia which was implicated in the formation of brown color and fluorescence. Among other nitrogen
donors tested (asparagine, glutamic acid and urea) our results demonstrated that free glutamine was a major source of ammonia
during heating. When heated at 120 and 180 °C, 100% of ammonia was released from glutamine after 60 and 10 min, respectively.
The second pathway involved a direct Maillard reaction with the α-amino group of glutamine. Both pathways led to a rapid and
complete destruction of glutamine when heated in the model systems. With reference to the Maillard browning (absorbance at
420 nm) glutamine turned out to be the most reactive amine, followed by asparagine, glutamate, ammonia and urea. Maximum fluorescence
(excitation and emission wavelengths at 330 and 450 nm, respectively) was also observed with glutamine followed by urea and
ammonia. Overall this study suggested that free glutamine predominantly contributes to the color and fluorescence formations
of foodstuffs. 相似文献
11.
Increased ethylene evolution accompanies seed germination of many species including Pisum sativum L., but only a little is known about the regulation of the ethylene biosynthetic pathway in different seed tissues. Biosynthesis
of the direct ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC), the expression of ACC oxidase (ACO), and ethylene
production were investigated in the cotyledons and embryonic axis of germinating pea seeds. An early onset and sequential
induction of ACC biosynthesis, accumulation of Ps-ACO1 mRNA and of ACO activity, and ethylene production were localized almost exclusively in the embryonic axis. Maximal levels
of ACC, Ps-ACO1 mRNA, ACO enzyme activity and ethylene evolution were found when radicle emergence was just complete. Treatment of germinating
seeds with ethylene alone or in combination with the inhibitor of ethylene action 2,5-norbornadiene showed that endogenous
ethylene regulates its own biosynthesis through a positive feedback loop that enhances ACO expression. Accumulation of Ps-ACO1 mRNA and of ACO enzyme activity in the embryonic axis during the late phase of germination required ethylene, whereas Ps-ACS1 mRNA levels and overall ACC contents were not induced by ethylene treatment. Ethylene did not induce ACO in the embryonic
axis during the early phase of germination. Ethylene-independent signalling pathways regulate the spatial and temporal pattern
of ethylene biosynthesis, whereas the ethylene signalling pathway regulates high-level ACO expression in the embryonic axis,
and thereby enhances ethylene evolution during seed germination.
Received: 28 September 1999 / Accepted: 27 December 1999 相似文献
12.
Focus on phosphohistidine 总被引:1,自引:0,他引:1
Summary. Phosphohistidine has been identified as an enzymic intermediate in numerous biochemical reactions and plays a functional role
in many regulatory pathways. Unlike the phosphoester bond of its cousins (phosphoserine, phosphothreonine and phosphotyrosine),
the phosphoramidate (P–N) bond of phosphohistidine has a high ΔG° of hydrolysis and is unstable under acidic conditions. This
acid-lability has meant that the study of protein histidine phosphorylation and the associated protein kinases has been slower
to progress than other protein phosphorylation studies.
Histidine phosphorylation is a crucial component of cell signalling in prokaryotes and lower eukaryotes. It is also now becoming
widely reported in mammalian signalling pathways and implicated in certain human disease states. This review covers the chemistry
of phosphohistidine in terms of its isomeric forms and chemical derivatives, how they can be synthesized, purified, identified
and the relative stabilities of each of these forms. Furthermore, we highlight how this chemistry relates to the role of phosphohistidine
in its various biological functions. 相似文献
13.
Biegel A Knütter I Hartrodt B Gebauer S Theis S Luckner P Kottra G Rastetter M Zebisch K Thondorf I Daniel H Neubert K Brandsch M 《Amino acids》2006,31(2):137-156
Summary. The H+/peptide cotransporter PEPT2 is expressed in a variety of organs including kidney, lung, brain, mammary gland, and eye. PEPT2
substrates are di- and tripeptides as well as peptidomimetics, such as β-lactam antibiotics. Due to the presence of PEPT2
at the bronchial epithelium, the aerosolic administration of peptide-like drugs might play a major role in future treatment
of various pulmonary and systemic diseases. Moreover, PEPT2 has a significant influence on the in vivo disposition and half-life
time of peptide-like drugs within the body, particularly in kidney and brain. PEPT2 is known to have similar but not identical
structural requirements for substrate recognition and transport compared to PEPT1, its intestinal counterpart. In this review
we compiled available affinity constants of 352 compounds, measured at different mammalian tissues and expression systems
and compare the data whenever possible with those of PEPT1. 相似文献
14.
Summary. Calcium ion (Ca2+) uptake was measured in rod outer segments (ROS) isolated from rat retina in the presence of varying concentrations of CaCl2 in the incubation buffer (1.0–2.5 mM). It is known that taurine increases Ca2+ uptake in rat ROS in the presence of ATP and at low concentrations of CaCl2 (Lombardini, 1985a); taurine produces no significant effects when CaCl2 concentrations are increased to 1.0 and 2.5 mM. With the removal of both taurine and ATP, Ca2+ uptake in rat ROS increased significantly in the presence of 2.5 mM CaCl2. Taurine treatment in the absence of ATP was effective in decreasing Ca2+ uptake at the higher levels of CaCl2 (2.0 and 2.5 mM). Similar effects were observed with ATP treatment. The data suggest that taurine and ATP, alone or in combination,
limit the capacity of the rat ROS to take up Ca2+ to the extent that a stable uptake level is achieved under conditions of increasing extracellular Ca2+, indicating a protective role for both agents against calcium toxicity.
Received January 25, 2000/Accepted January 31, 2000 相似文献
15.
Summary. The effect of α-difluoromethylornithine (DFMO) on the apoptosis of HC11 mouse mammary epithelial cells was investigated.
The involvement of reactive oxygen species (ROS) and Bcl-2 protein in the mechanism of apoptosis induced by ornithine decarboxylase
(ODC) inhibition was also assessed. DFMO (0.1, 1 and 5 mM) induced apoptosis of HC11 cells in dose- and time-dependent manner.
Apoptosis manifests itself with morphological features like: cell shrinkage, condensation of chromatin, pyknosis and fragmentation
of nucleus, followed by secondary necrosis (putrosis). The decrease in the nuclear DNA contents appearing as the hypodiploidal
peak sub-G1 in the DNA histogram was not dependent on the presence of prolactin (5 μg/ml) in DFMO-treated cultures. Apoptosis induced
by ODC inhibition was associated with a rapid increase in ROS concentration in HC11 cells observed within 1 h after DFMO treatment.
The down-regulation of Bcl-2 as a decrease in cell number expressing bcl-2 and a lowered Bcl-2 protein content in cells expressing this protooncogene was also noted. The administration of putrescine
(50 μM) lowered the number of early-apoptotic, late-apoptotic and necrotic cells. Moreover, it increased the number of cells
expressing bcl-2. In conclusion, the disturbance of cellular polyamine homeostasis by inhibition of their synthesis enhances mammary epithelial
cell susceptibility to apoptosis. It may occur in the mammary gland at the end of lactation, when the depletion of circulating
lactogenic hormones and activation of intra-mammary apoptogenic factors expression take place.
Received May 6, 1999; Accepted December 15, 1999 相似文献
16.
Catabolism of native and oxidized low density lipoproteins: in vivo insights from small animal positron emission tomography studies 总被引:5,自引:0,他引:5
Summary. The human organism is exposed to numerous processes that generate reactive oxygen species (ROS). ROS may directly or indirectly
cause oxidative modification and damage of proteins. Protein oxidation is regarded as a crucial event in the pathogenesis
of various diseases ranging from rheumatoid arthritis to Alzheimer’s disease and atherosclerosis. As a representative example,
oxidation of low density lipoprotein (LDL) is regarded as a crucial event in atherogenesis. Data concerning the role of circulating
oxidized LDL (oxLDL) in the development and outcome of diseases are scarce. One reason for this is the shortage of methods
for direct assessment of the metabolic fate of circulating oxLDL in vivo. We present an improved methodology based on the radiolabelling of apoB-100 of native LDL (nLDL) and oxLDL, respectively,
with the positron emitter fluorine-18 (18F) by conjugation with N-succinimidyl-4-[18F]fluorobenzoate ([18F]SFB). Radiolabelling of both nLDL and oxLDL using [18F]SFB causes neither additional oxidative structural modifications of LDL lipids and proteins nor alteration of their biological
activity and functionality, respectively, in vitro. The method was further evaluated with respect to the radiopharmacological properties of both [18F]fluorobenzoylated nLDL and oxLDL by biodistribution studies in male Wistar rats. The metabolic fate of [18F]fluorobenzoylated nLDL and oxLDL in rats in vivo was further delineated by dynamic positron emission tomography (PET) using a dedicated small animal tomograph (spatial resolution
of 2 mm). From this study we conclude that the use of [18F]FB-labelled LDL particles is an attractive alternative to, e.g., LDL iodination methods, and is of value to characterize
and to discriminate the kinetics and the metabolic fate of nLDL and oxLDL in small animals in vivo. 相似文献
17.
Trog D Moenkemann H Breipohl W Schueller H Schild H Golubnitschaja O 《Amino acids》2007,32(3):373-379
Summary.
Objectives. Human gliomas have a catastrophic prognosis with a median survival in the range of one year even after therapeutic treatment.
Relatively high resistance towards apoptotic stimuli is the characteristic feature of malignant gliomas. Since cell cycle
control has been shown to be the key mechanism controlling both apoptosis and proliferation, this study focuses on DNA damage
analysis and protein expression patterns of essential cell cycle regulators P53 and P21waf1/cip1 in glioma under clinically relevant therapeutic conditions.
Material and methods. U87MG cell line, characterised by wild p53-phenotype relevant for the majority of primary malignant glioblastomas, was used. Glioma cells underwent either irradiation
or temozolomide treatment alone, or combined radio/chemo treatment. DNA damage was analysed by the “Comet Assay”. Expression
rates of target proteins were analysed using “Western-Blot” technique.
Results and conclusions. “Comet Assay” demonstrated extensive DNA damage caused by temozolomide treatment alone and in combination with irradiation,
correlating well with the low survival rate observed under these treatment conditions. In contrast, irradiation alone resulted
in a relatively low DNA damage, correlating well with a high survival rate and indicating a poor therapeutic efficiency of
irradiation alone. Unusually low up-regulation of P53 and P21waf1/cip1 expression patterns was produced by the hereby tested stressful conditions. A deficit in cell cycle control might be the
clue to the high resistance of malignant glioma cells to established therapeutic approaches. 相似文献
18.
Nikolic J Stojanovic I Pavlovic R Sokolovic D Bjelakovic G Beninati S 《Amino acids》2007,32(1):127-131
Summary. The existing interrelation in metabolic pathways of L-arginine to polyamines, nitric oxide (NO) and urea synthesis could be
affected in sepsis, inflammation, intoxication and other conditions. The role of polyamines and NO in the toxic effect of
mercury chloride on rat liver function was studied. Administration of mercury chloride for 24 h led to significantly elevated
plasma activities of Alanine transaminase (ALT) and Aspartate transaminase (AST). Malondyaldehyde (MDA) levels were unaffected
(p > 0.05) and arginase activity was significantly decreased (p < 0.05) while nitrate/nitrite production was significantly
elevated (p < 0.001) in liver tissue. Polyamine oxidase (PAO) and diamine oxidase (DAO) activities, enzymes involved in catabolism
of polyamines, were decreased. L-arginine supplementation to intoxicated rats potentiated the effect of mercury chloride on
NO production and it was ineffective on arginase activity.
Results obtained in this study show that mercury chloride-induced toxicity leads to abnormally high levels of ALT and AST
that may indicate liver damage with the involvement of polyamine catabolic enzymes and NO. 相似文献
19.
Taranukhin AG Taranukhina EY Saransaari P Djatchkova IM Pelto-Huikko M Oja SS 《Amino acids》2008,34(1):169-174
Summary. Taurine is a sulphur-containing amino acid abundant in the nervous system. It protects cells from ischemia-induced apoptosis,
but the mechanism underlying this is not well established. The aim of our study was to explore the effects of taurine on two
main pathways of apoptosis induced by ischemia: receptor-mediated and mitochondrial cell death. Brain slices containing the
supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus were incubated in vitro under control and simulated
ischemic (oxygen-glucose deprivation for 30 min) conditions in the absence and presence of 20 mM taurine. Brain slices were
harvested after the 180-min “postischemic” period and fixed in 4% paraformaldehyde. To estimate apoptosis, immunostaining
was done for caspase-8 and caspase-9 in paraffin-embedded sections. Immunoreactive caspase-8 and caspase-9 cells were observed
in SON and PVN in all experimental groups, but in the “ischemic” group the expression of caspase-8 and caspase-9 and the number
of immunoreactive cells was significantly increased in both hypothalamic nuclei. Addition of taurine (20 mM) to the incubation
medium induced a marked decrease in caspase-8 and caspase-9 immunoreactivity after ischemia in SON and PVN when compared with
the taurine-untreated “ischemic” group. Taurine reduces ischemia-induced caspase-8 and caspase-9 expression, the key inductors
of apoptosis in SON and PVN.
Authors’ address: Dr. Andrey Taranukhin, Tampere Brain Research Center, Medical School, University of Tampere, FI-33014 Finland 相似文献
20.
Batch cultures of photoautotrophic cell suspensions of Chenopodiumrubrum L., growing in an inorganic medium on CO2 under a daily balanced light–dark regime of 16 : 8 h could be maintained for approximately 100 d without subcultivation.
The long-lived cultures showed an initial cell division phase of 4 weeks, followed by a stationary phase of another 4 weeks,
after which ageing and progressive cell death reduced the number of living cells and the cultures usually expired after another
3–4 weeks. These developmental phases of the cell culture were characterised with respect to photosynthetic performance, dark
respiration, content of phytohormones and capacity of cell division. Cell division of the majority of the cells finished in
the G1- or G0-phase of the cell cycle, caused by a pronounced decline in the endogenous levels of auxin and cytokinins. Supply
of these growth factors to resting cells resulted in resumption of cytokinesis, at least by some of the cells. However, responsiveness
to the phytohomones declined during the stationary phase, and subcultivation was no longer possible beyond day 60 when the
phases of ageing and death commenced. Ageing was characterised by a further decline in the photosynthetic capacity of the
cells, by a climacteric enhancement of dark respiration, but also by a slight increase in the level of IAA and cytokinins
concomitant with a decrease in ethylene. Similarities and differences between the development of batch-cultured photoautotrophic
cells of C. rubrum and that of a leaf are discussed with respect to using the cell culture as a model for a leaf.
Received: 30 April 1999 / Accepted: 21 August 1999 相似文献