According to traditional Chinese medicine , Cordyceps sinensis (CS) can prevent subjects from renal failure. The aim of this study was to investigate the protective effect of CS preconditioning on ischemic renal acute failure in rats and to assess its mechanism. The animal model of ischemic acute renal failure was performed by left nephrectomy and clamping right renal vessel for 45 mins in S-D rats. Cordyceps group had been pretreated with two-day 600 mg/kg CS before I/R injury. Rats were sacrificed at 1, 3, 6, 16, 48 and 120 h after reperfusion for evaluation of renal function and histopathological PASD staining. The immunohistochemistry and Western blotting of SDF-1£\, CXCR4 and Ki67 were also performed. £E-galactosidase activity was detected with the senescence staining. The results showed that the level of creatinine in Cordyceps group were significant lower after 48 hours I/R injury (p =0.04). PSAD staining in Cordyceps group revealed less tubular necrosis, tubular dilatation, and cast formation at 6 and 16 hour than in control group. Immunohistochemistry of SDF-1£\ in Cordyceps group demonstrated staining in the distal tubules and collecting ducts at 1, 3, 6, and 16 h. The CXCR4 signal of control group had gradually intensified from 1 to 6 hr after I/R . In Cordyceps group, the CXCR4 expression had been stabilized until 16 h after I/R. The £]-galactosidase activity was higher in control group at 1, 3 and 6 hours. However, the senescence was presented at 1 and 3 hours in Cordyceps group. The nuclear staining of repair enzyme Ki67 in Cordyceps group showed higher density than in control group. Pathologic morphology indicated CS may protect subjects from ischemic acute renal failure. CS also induced SDF-1£\ expression in early stage of I/R injury, and maintained the stable CXCR4 expression. CS can not only reduce the activity of senescence-related £]-galactosidase, but also regulate the expression of repair enzyme Ki67, indicating that CS may alleviate the ischemic-induced senescence and enhance renal repair.

Ethylene is a plant growth regulator and plays a key role in leaf senescence. Its signaling, however, remains mostly unclear in sweet potato. Ethephon, an ethylene releasing compound, induced sweet potato detached leaf senescence and associated gene expression, and the effects were repressed by mitogen-activated protein kinase (MAPK) kinase inhibitor PD98059. These data suggest that MAPK cascade is likely involved in ethylene signaling leading to leaf senescence and associated gene expression. With gene-specific primers and RT-PCR methods, a full-length cDNA, SPMAPK, was isolated from ethephon-treated sweet potato leaves. SPMAPK contained 1098 nucleotides (365 amino acids) in the open reading frame. Sweet potato SPMAPK also exhibited high amino acid sequence identities (ca. 79.8% to 83.4%) with plant MAPKs, and was most close to Arabidopsis MPK3 and MPK6 in phylogenetic tree analysis. RT-PCR analysis showed that SPMAPK gene expression was detected in roots, stems, and leaves. The mature and partial yellowing leaves expressed higher amount. SPMAPK gene expression was also inducible and significantly enhanced by ethephon. Results from studies with inhibitors or effectors showed that ethephon treatment resulted in acceleration of leaf senescence in detached sweet potato leaves, promotion of leaf chlorophyll content reduction and decrease of photochemical Fv/Fm, and induction of associated gene expression. These ethephon-mediated effects were all delayed or repressed by pretreatment with ethylene receptor inhibitor 1-methylcyclopropene (1-MCP), MAPK kinase inhibitor PD98059, NADPH oxidase inhibitor diphenyleneiodonium (DPI), antioxidant reduced glutathione, calcium ion chelator EGTA, and de novo protein synthesis inhibitor cycloheximide, respectively. Based on these results we conclude that an ethylene-inducible mitogen-activated protein kinase SPMAPK was isolated from sweet potato leaves, and expressed higher amount in mature and partial yellowing leaves. Ethephon-induced sweet potato SPMAPK expression was significantly repressed by 1-MCP, PD98059, DPI, reduced glutathione, EGTA and cycloheximide. These data also suggest that the possible signal components in ethephon-mediated leaf senescence and associated gene expression in sweet potato leaves likely include ethylene receptor, MAPK cascade, elevated H2O2 , external calcium influx, and de novo synthesized proteins. A possible ethylene signaling model leading to sweet potato leaf senescence and associated gene expression was also proposed.

Ethylene is a gaseous growth regulator, and plays an important role in response to plant developmental and environmental stimuli. Ethylene also plays a key role in leaf senescence. Calcium is a second message, and participates in the signal transduction pathways of many plant physiological responses. In this research, ethephon, an ethylene-releasing compound, was used to induce sweet potato leaf yellowing, chlorophyll content reduction, photochemical Fv/Fm decrease, H2O2 elevation and senescence-associated gene expression. These ethephon-mediated effects were all delayed or repressed by pretreatment of a calcium ion chelator, EGTA. Treatment with a calcium ionophore A23187 also induced senescence-associated gene expression in sweet potato detached leaves, and the induction was repressed by EGTA pretreatment. Calcium signaling in general is transmitted by calcium sensor proteins, including calmodulin to translate into appropriate responses to developmental and environmental stimuli. Therefore, pretreatment with calmodulin inhibitor chlorpromazine (CPZ) delayed or repressed ethephon-mediated leaf senescence, H2O2 elevation and senescence-associated gene expression. These CPZ-mediated effects were reversed by the exogenous application of an ethephon-inducible calmodulin SPCAM fusion protein. These results suggest that external Ca2+ influx and calmodulin SPCAM play a role in ethephon signaling leading to leaf senescence, H2O2 elevation and senescence-associated gene expression. In addition, NaCl salt stress also caused sweet potato leaf senescence, H2O2 elevation and senescence-associated gene expression. Pretreatment with CPZ delayed or repressed NaCl salt stress-mediated leaf senescence, H2O2 elevation and senescence-associated gene expression. These CPZ-mediated effects were also reversed by the exogenous application of calmodulin SPCAM fusion protein. These results suggest that calmodulin SPCAM may play a role in NaCl salt stress signaling leading to leaf senescence, H2O2 elevation and senescence-associated gene expression. Based on these results, external Ca2+ influx is required for ethephon induced leaf senescence. Ethephon-inducible calmodulin SPCAM likely participates in ethylene and NaCl salt stress signaling leading to leaf senescence, H2O2 elevation and senescence-associated gene expression in sweet potato in order to cope with different developmental cues or environmental stimuli.

Ethylene has long been considered as the main plant growth regulator that plays a key role in the regulation of leaf senescence. In sweet potato, ethephon, an ethylene releasing compound, promoted leaf senescence and H2O2 elevation. These ethephon-mediated effects were alleviated or attenuated by exogenous reduced glutathione and ascorbic acid. Ethephon treatment gradually increased endogenous total and reduced glutathione and ascorbic acid levels in sweet potato detached leaves 3 days after treatment. The H2O2 amount, however, was also increased at 72 h after treatment. Sweet potato detached leaves pretreated with reduced glutathione did significantly increased endogenous total and reduced glutathione levels at 24 h and remarkably decreased H2O2 amount at 72 h after ethephon application compared to that of ethephon alone control. Ethephon caused quick elevation of a small H2O2 peak at about 4 h after application, and the enhancement was eliminated by reduced glutathione pretreatment in treated sweet potato leaves. Pretreatment of diphenylene iodonium (DPI), an NADPH oxidase inhibitor, also repressed leaf senescence and H2O2 elevation at day 3 after ethephon treatment in sweet potato detached leaves, and the attenuation was effective within the first 4 h after ethephon treatment. For senescence-associated gene expression, ethephon and L-buthionine sulfoximine (BSO), an endogenous glutathione synthase inhibitor, did induced asparaginyl endopeptidase (SPAE) and cysteine proteases (SPCP1, SPCP2 and SPCP3) gene expression and the activation was repressed by reduced glutathione pretreatment. Based on these data we conclude that ethephon treatment may cause quick elevation of a small H2O2 peak likely via the NADPH oxidase, which may function as a signal component leading to leaf senescence, H2O2 elevation and senescence-associated gene expression in sweet potato detached leaves. The rate of endogenous antioxidant such as reduced glutathione elevation is also important and affects leaf senescence, H2O2 elevation and senescence-associated gene expression in sweet potato leaves.

<p>Complications from cardiovascular disease, such as a heart attack or a stroke, represent the leading cause of death in the United States and many developed and developing countries. Atherosclerosis is the primary pathology underlying cardiovascular disease. It is caused by an increase in endothelial cell (EC) permeability, leading to the buildup of cholesterol and lipids which form the atherosclerotic plaque. Accelerated aging in regions of atherosclerosis contribute to the development and progression of the disease. The global hypothesis that motivated this research was that activation of deacetylase antioxidant regulator, Sirtuin1 (SIRT1), improved function in senescent endothelial cells ECs by increasing the integrity of cell-cell junctions. In turn, this led to elevated EC permeability, a decline in the response to shear stress, and elevated traction forces.</p><p>Aging of hCB-ECs significantly increased permeability due to changes in tight junction protein localization and phosphorylation. Activation of SIRT1 significantly reduced permeability in aged hCB-ECs and restored junction integrity. ECs under flow also exhibited changes in cell junctions with increasing age. Aged hCB-ECs were less responsive to shear stress, exhibiting lower levels of atheroprotective genes, KLF2 and eNOS. Activation of SIRT1 in aged hCB-ECs restored the response to shear stress by altering localization and phosphorylation of adherens junction protein, VE-cadherin. The endothelial glycocalyx is a layer of proteoglycans and glycoproteins on the surface of ECs that is important in maintaining EC barrier function. In aging ECs, the glycocalyx was thinner and less dense. However, activation of SIRT1 restored the structure of the glycocalyx, suggesting that the positive effect of SIRT1 on elevated permeability in aged hCB-ECs may also be due to restoration of the glycocalyx. Aged hCB-ECs also exhibited elevated traction forces for measurements done with single cells, cell clusters (2 to 3 cells), and cell monolayers (20 to 30 cells). The elevated traction forces correlated with altered actin localization and increased actin filament thickness. Activation of SIRT1 reduced traction forces and decreased actin stress fiber thickness in aged hCB-ECs, suggesting that the effects of SIRT1 on cell-cell junctions alters binding of junction proteins to the actin cytoskeleton and generation of cell traction forces. Together, these results implicate an important role for SIRT1 in regulating permeability and mechanotransduction in aging endothelium.</p> / Dissertation

Worldwide, people are being exposed to natural and man-made sources of radiation. Epidemiological studies have shown an increased risk of vascular diseases in populations that have been exposed to ionizing radiation. Vascular endothelium is implicated as one of the targets for radiation leading to the development of cardiovascular diseases. However, the molecular mechanisms behind the development of radiation-induced cardiovascular disease in acute or chronic exposed people are not fully elucidated. The hypothesis that chronic low dose rate ionizing radiation accelerates the onset of senescence of primary human umbilical vein endothelial cells has been tested in papers I and II presented in this thesis. In vitro studies show that, when exposed to continuous low dose rate gamma radiation these cells enter premature senescence much earlier than non-irradiated control cells. Quantitative proteomic analysis using isotope coded protein labeling coupled to LC-ESI-mass spectrometry and followed by protein network analysis identified changes in senescence-related biological pathways including cytoskeletal organisation, cell-cell communication and adhesion, and inflammation influenced by radiation. Moreover, the role of PI3K/Akt/mTOR pathway was implicated during the senescence process. Thus, chronic low dose rated endothelial senescence may contribute to increased risk of radiation-induced cardiovascular disease. Paper III analyse the long-term effects of local high doses of radiation to the heart using a mouse model. The results from proteomic and bioinformatics analysis indicated that an impaired activity of the peroxisome proliferator-activated receptor-alpha (PPARA) is involved in mediating the radiation response. Ionizing radiation markedly changed the phosphorylation and ubiquitination status of PPARA. This was reflected by the decreased expression of PPARA target genes involved in energy metabolism and mitochondrial respiratory chain. This in vivo study suggests that alteration of cardiac metabolism contributes to the impairment of heart structure and function after radiation. Taken together, these in vitro and in vivo studies provide novel information on the pathways in heart and endothelial cells that are affected over longer periods of time by ionizing radiation.

Ageing reduces fitness, but how ageing evolves is still unclear. Evolutionary theory of ageing hinges on the fundamental principal that the force of natural selection declines with age. This principle has yielded two important predictions: 1) the evolution of faster ageing in populations under high rate of extrinsic mortality; and 2) the evolution of faster ageing in a sex that experiences higher rates of extrinsic mortality. However, an emerging new theory argues that when the extrinsic mortality is not random but instead selects on traits showing positive genetic correlation with lifespan, increased mortality should lead to the evolution of increased lifespan. Such condition-dependent mortality is also expected to increase the robustness in the population, resulting in increased deceleration of mortality in late-life. Similarly, high sex-specific mortality can result in increased sex-specific selection on traits that have positive pleiotropic effects on lifespan in the affected sex. This thesis is based on two experimental evolution studies in Caenorhabditis remanei. The first experiment was designed to disentangle the effects of the rate (high or low) and the source (random or condition-dependent) of mortality on the evolution of lifespan and ageing. Reduced lifespan evolved under high rate of random mortality, whereas high condition-dependent mortality, imposed by heat-shock, led to the evolution of increased lifespan (Paper I). However, while female reproduction increased under condition-dependent mortality, male reproduction suffered, suggesting a role for sexual antagonism in maintaining genetic variation for fitness (Paper II). Besides, long lifespan and high fecundity evolved at a cost of slow juvenile growth rate in females (Paper III). Moreover, high condition-dependent mortality led to the evolution of lower rate of intrinsic mortality in late-life (Paper IV). The second experiment showed that evolution of sexual dimorphism in lifespan is driven by the factors that cause sex-specific mortality and cannot be predicted from differences in mortality rate alone. Specifically, high condition-dependent mortality renders males less prone to ageing than females despite higher rates of male mortality (Paper V). The strength of this thesis is the reconfirmation of the earlier findings combined with support for the new theory. Rather than further complicating the matter, the inclusion of the new ideas should help explain some empirical results that are inconsistent with the classic theory, as well as provide a more comprehensive picture of ageing evolution.

333f. / Submitted by Suelen Reis (suziy.ellen@gmail.com) on 2013-04-22T17:10:30Z No. of bitstreams: 7 Tese Katia Bernardo7.pdf: 6922729 bytes, checksum: 415a54b477c67ae1e0ea2dc40ff9f095 (MD5) Tese Katia Bernardo6.pdf: 7071403 bytes, checksum: 5c20435e72b54770be45263b35cac822 (MD5) Tese Katia Bernardo5.pdf: 6623770 bytes, checksum: a01defc168d6ca8cc0f29661a03540ed (MD5) Tese Katia Bernardo4.pdf: 6444867 bytes, checksum: 8c604618251a966bf55ec1c0e53a670f (MD5) Tese Katia Bernardo3.pdf: 2128356 bytes, checksum: 6032a215ef027999e988395cff274e03 (MD5) Tese Katia Bernardo2.pdf: 6708255 bytes, checksum: 77d68555d85d22482449dbc0cd40b6a8 (MD5) Tese Katia Bernardo1.pdf: 7208484 bytes, checksum: 7161a8792d1a6331aac14f3dfda27ce0 (MD5) / Approved for entry into archive by Rodrigo Meirelles(rodrigomei@ufba.br) on 2013-05-24T11:34:21Z (GMT) No. of bitstreams: 7 Tese Katia Bernardo7.pdf: 6922729 bytes, checksum: 415a54b477c67ae1e0ea2dc40ff9f095 (MD5) Tese Katia Bernardo6.pdf: 7071403 bytes, checksum: 5c20435e72b54770be45263b35cac822 (MD5) Tese Katia Bernardo5.pdf: 6623770 bytes, checksum: a01defc168d6ca8cc0f29661a03540ed (MD5) Tese Katia Bernardo4.pdf: 6444867 bytes, checksum: 8c604618251a966bf55ec1c0e53a670f (MD5) Tese Katia Bernardo3.pdf: 2128356 bytes, checksum: 6032a215ef027999e988395cff274e03 (MD5) Tese Katia Bernardo2.pdf: 6708255 bytes, checksum: 77d68555d85d22482449dbc0cd40b6a8 (MD5) Tese Katia Bernardo1.pdf: 7208484 bytes, checksum: 7161a8792d1a6331aac14f3dfda27ce0 (MD5) / Made available in DSpace on 2013-05-24T11:34:21Z (GMT). No. of bitstreams: 7 Tese Katia Bernardo7.pdf: 6922729 bytes, checksum: 415a54b477c67ae1e0ea2dc40ff9f095 (MD5) Tese Katia Bernardo6.pdf: 7071403 bytes, checksum: 5c20435e72b54770be45263b35cac822 (MD5) Tese Katia Bernardo5.pdf: 6623770 bytes, checksum: a01defc168d6ca8cc0f29661a03540ed (MD5) Tese Katia Bernardo4.pdf: 6444867 bytes, checksum: 8c604618251a966bf55ec1c0e53a670f (MD5) Tese Katia Bernardo3.pdf: 2128356 bytes, checksum: 6032a215ef027999e988395cff274e03 (MD5) Tese Katia Bernardo2.pdf: 6708255 bytes, checksum: 77d68555d85d22482449dbc0cd40b6a8 (MD5) Tese Katia Bernardo1.pdf: 7208484 bytes, checksum: 7161a8792d1a6331aac14f3dfda27ce0 (MD5) Previous issue date: 2010 / O envelhecimento é uma etapa da vida humana que atinge diferentemente os indivíduos de acordo com sua condição social, gênero e cor da pele. Mediante a reconstrução histórica de Salvador na segunda metade do século XIX e dos contextos onde estavam os sujeitos da pesquisa, busca-se identificar o posicionamento das Instituições governamentais e privadas em relação ao tratamento reservado ao segmento da população formado pelos velhos; indicar as práticas e os mecanismos sociais por meio dos quais as posições sociais desses personagens foram estabelecidas e suas diferenças legitimadas; analisar o contexto de institucionalização da velhice, buscando estabelecer relações entre esse evento, a emergência da pobreza como questão social em Salvador e o caráter de caridade e de mendicidade no tratamento dado aos velhos; evidenciar os fundamentos dos modelos asilares, avaliando a qualidade da estrutura desses espaços no referido período; discutir a presença das relações de gênero e raça no tratamento dado à velhice. Acreditando que a observação microscópica revelaria fatores previamente não observados, utilizou-se o referencial teórico e metodológico da Micro-História durante o desenvolvimento da pesquisa. Os resultados permitiram verificar-se que, na segunda metade do século XIX, a velhice não fazia parte das agendas públicas e era objeto de filantropia e piedade ou um problema de família; a população idosa que morava em Salvador formava um grupo heterogêneo e complexo; era composta por pessoas cujo intervalo de idade ultrapassava 30 anos e experimentaram trajetórias de vida diferenciada; e, ao contrário do que se costuma pensar, a longevidade não é um fenômeno recente, mas vem ocorrendo, paulatinamente, desde a segunda metade do século XIX, quando um contingente significativo de pessoas tornou-se longevo. Constatamos que, apesar de todo o avanço da capital da Província, ela era perigosa para os velhos que nela transitavam, seja pelos riscos de atropelos provocados pelos novos meios de transporte, pela pouca iluminação das ruas ou pela sujeira decorrente da falta de saneamento básico, que tornava as ruas esgotos a céu aberto, infestadas por repetidas epidemias de febre amarela e de cólera. Verificou-se que a sociedade baiana oitocentista via a velhice como uma fase de decadência e decrepitude. O contexto do surgimento dos asilos explica, de alguma forma, a representação social negativa da velhice: pessoas idosas misturadas aos diversos tipos sociais. As relações de gênero e raça expunham diferenças de tratamento em ambos os casos; havia diferença de tratamento para homens e mulheres brancos idosos. Um aspecto que mereceu destaque foi o número de idosos que morreram trabalhando, independente de classe social, gênero ou raça, a despeito da manutenção, no imaginário social, da velhice como uma fase improdutiva, devido à incapacidade para o trabalho e do surgimento de limitações físicas e mentais. Concluiu-se que a velhice, longe de ser uma categoria natural, é um fenômeno construído socialmente, já que o grupo constituído pelos idosos não é homogêneo, mas fortemente marcado pelas relações de gênero, classe social e etnia/raça. Acima de tudo, ao se pensar o envelhecimento, não se pode esquecer que o contexto influi de maneira significativa nas diversas formas de velhice. / Salvador

Made available in DSpace on 2015-09-17T15:25:44Z (GMT). No. of bitstreams: 0 Previous issue date: 2015-03-18. Added 1 bitstream(s) on 2015-09-17T15:46:37Z : No. of bitstreams: 1 000846277.pdf: 2026141 bytes, checksum: 0bb21e6aa2c7922e2a387ecf5fd901d7 (MD5) / The age as well as the presence of inflammation can influence the cellular metabolism, slowing the tissue healing process. Different therapies, such as the application of growth factors and low level laser therapy (LLLT) are capable of biostimulating cells by increasing their proliferation and metabolism. The aim of this study was to evaluate: the functions of gingival fibroblasts obtained from young and elderly individuals (Study 1); the response of these cells exposed to tumor necrosis factor alpha - TNF-α (Study 2); and the effect of LLLT or epidermal growth factor - EGF on the viability and metabolism of these connective cell type (Study 3). Primary culture of gingival fibroblasts of 6 patients (3 young - Y and 3 elderly - E) were collected and cultured in complete culture medium (DMEM). In the Study 1 fibroblasts were seeded in 96-well plates in complete DMEM containing 10% of fetal bovine serum (FBS) for 24, 48 or 72 hours and subjected to evaluation of cell viability (MTT, n=36), total protein production (TP, n=36) and collagen synthesis (SR, n=36). In the Study 2, after 24-hour cell seeding, the complete DMEM was replaced by DMEM without FBS supplemented or not with TNF-α (100 ng/mL) which was kept in contact with cells for additional 24 hours. Then, the production of reactive oxygen TNF-α species (ROS, n=36), nitric oxide (NO, n=36) and synthesis of CCL5 chemokine (ELISA, n=36) were assessed. In the Study 3 fibroblasts were seeded in 24-well plates for 24 hours, and then exposed to EGF (100 μM) or submitted to low power laser irradiation (LASERTable device, InGaAsP - 780 ± 3nm; 25mW). Cell viability (Alamar Blue®, n=12), cell migration (Wound Healing, n=12), collagen synthesis (SR, n=12), and synthesis of vascular endothelial growth factor - VEGF (ELISA, n=12) were assessed 72 hours after the treatments. The data were statistical...(Complete abstract electronic access below)

Orientador: Giuseppina Pace Pereira Lima / Banca: João Domingos Rodrigues / Banca: Armando Reis Tavares / Resumo: A produção de flores de corte constitui uma atividade promissora, cuja comercialização exige técnicas de conservação que contribuem em manter a qualidade floral pós-colheita. A giberelina é um regulador vegetal que apresenta grande eficiência no crescimento, na indução de florescimento, na brotação, pode retardar a senescência, entre outros. Assim, o objetivo deste trabalho foi avaliar o efeito de baixas concentrações de ácido giberélico (GA3) aplicado a campo no crescimento da flor e qualidade pós-colheita de crisântemo cv. 'Faroe'. As plantas foram pulverizadas aos 28 (vinte e oito) dias após o transplantio das mudas e a colheita programada com 95% das lígulas expandidas. Após a colheita, foram medidos os parâmetros: altura e diâmetro da haste, diâmetro da flor, comprimento da lígula, número de flores e tempo de reação (indução ao florescimento). Após a avaliação, as hastes foram armazenadas em câmara fria a temperatura de 10 °C e UR 95% durante 48 horas e levadas à temperatura ambiente. Após o periodo de armazenamento em câmara fria, foram comparadas com as hastes mantidas em temperatura ambiente e submetidas às seguintes análises: avaliação da senescência floral (escala de notas), consumo da solução do recipiente e medida do pH, ambas em intervalos de dois dias. A qualidade das hastes foi acompanhada pelas as análises bioquímicas (protéinas totais, carboidratos totais solúveis, atividade da peroxidase e poliaminas livres) no intervalo de quatro dias durante o tempo de vida de vaso. Apenas uma única aplicação de GA3 não teve interferência nas características fenotípicas em plantas de crisântemo cv 'Faroe', pelo menos em baixas concentrações, assim como não promoveram incremento na qualidade pós-colheita das flores. Não foi observado melhoria na qualidade das flores armazenadas ...(Resumo completo, clicar acesso eletrônico abaixo) / Abstract: The production of cut flowers is a promising commercial activity and its business demands conservation techniques that contribute to keep the post-harvested flower quality. Gibberellin is a growth regulator that is very efficient in the growth, flowering induction, budding, senescence delay, etc. Thus, the aim of this paper was to evaluate the effect of low concentrations of gibberellic acid (GA3) applied under field conditions on flower growth and post-harvest quality of chrysanthemums cv. 'Faroe'. Application was carried out at 28 days after seedling transplanting and harvest was scheduled when 95% of ligulas were expanded. The following parameters were measured after harvest: stem height and diameter, flower diameter, ligula length, number of flowers and reaction time (flowering induction). After evaluation, the stems were stored in a cold chamber at 10° C and relative humidity of 95% for 48 hours and then taken to room temperature. Later they were compared to the stems kept at room temperature and submitted to the following analyses: flower senescence evaluation (score scale), solution consume, pH measurement, both at 2-day intervals. Stem quality was evaluated through biochemical analysis (total proteins, total soluble carbohydrates, peroxidase activity and free polyamines) at four-day intervals during the vase life. A single low concentration GA3 application has not interfered on phenotypic characteristics of chrysanthemum cv. 'Faroe' plants neither has improved post-harvested flower quality. There was not quality improvement of flowers stored in cold chamber after stem exposure to room temperature and flower senescence evaluation. In both treatments, stems presented a higher solution consume and pH varied during the vase life. Stems kept at room temperature showed great decreases in total protein content as well as in total soluble carbohydrate content in leaves and flowers of chrysanthemum cv. Faroe. There was an increase ... / Mestre