Oxidative damage to mitochondria is a preliminary step to caspase-3 activation in fluoride-induced apoptosis in HL-60 cells

Anuradha, C. D.; Kanno, Sanae; Hirano, Seishiro

doi:10.1016/s0891-5849(01)00591-3

Cited by 205 publications

(116 citation statements)

References 42 publications

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“…Our result is consistent with sodium fluoride (NaF)-mediated apoptosis of HL-60 cells where the levels of ROS are elevated just after 3 h of exposure whereas the membrane potential is lost after 8 h of drug treatment. 29 One of the most important cellular defences against intracellular oxidative stress is GSH, which plays a critical role in mediating apoptosis in eukaryotes including leishmanial cells. A decrease in GSH level causes an increase in the number of CPT-induced DNA-protein crosslinks, indicating that GSH affects the mechanism of action of CPT.…”

Section: Discussionmentioning

confidence: 99%

“…[27][28][29] We have shown by Western blotting and confocal microscopy that CPT treatment causes cytochrome c accumulation in the cytoplasm ( Figure 6). A small amount of cytochrome c is present in the cytoplasmic fraction of the control promastigotes, but cytochrome c is abundant in the cytoplasmic fraction of CPT-treated cells.…”

Section: Loss Of Mitochondrial Membrane Potential Causes Release Of Cmentioning

confidence: 99%

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Camptothecin induced mitochondrial dysfunction leading to programmed cell death in unicellular hemoflagellate Leishmania donovani

et al. 2004

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The parasites of the order kinetoplastidae including Leishmania spp. emerge from most ancient phylogenic branches of unicellular eukaryotic lineages. In their life cycle, topoisomerase I plays a significant role in carrying out vital cellular processes. Camptothecin (CPT), an inhibitor of DNA topoisomerase I, induces programmed cell death (PCD) both in the amastigotes and promastigotes form of L. donovani parasites. CPT-induced cellular dysfunction in L. donovani promastigotes is characterized by several cytoplasmic and nuclear features of apoptosis. CPT inhibits cellular respiration that results in mitochondrial hyperpolarization taking place by oligomycin-sensitive F0-F1 ATPase-like protein in leishmanial cells. During the early phase of activation, there is an increase in reactive oxygen species (ROS) inside cells, which causes subsequent elevation in the level of lipid peroxidation and decrease in reducing equivalents like GSH. Endogenous ROS formation and lipid peroxidation cause eventual loss of mitochondrial membrane potential. Furthermore, cytochrome c is released into the cytosol in a manner independent of involvement of CED3/CPP32 group of proteases and unlike mammalian cells it is insensitive to cyclosporin A. These events are followed by activation of both CED3/CPP32 and ICE group of proteases in PCD of Leishmania. Taken together, our study indicates that different biochemical events leading to apoptosis in leishmanial cells provide information that could be exploited to develop newer potential therapeutic targets.

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Section: Discussionmentioning

confidence: 99%

Section: Loss Of Mitochondrial Membrane Potential Causes Release Of Cmentioning

confidence: 99%

Camptothecin induced mitochondrial dysfunction leading to programmed cell death in unicellular hemoflagellate Leishmania donovani

et al. 2004

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“…NaF, the first and still-recommended fluoride compound used for fluoridation of drinking water, was able to induce morphological and neoplastic transformation of Syrian hamster embryo cells 11,15 , as well as to increase chromosomal aberrations in CHO cells 1 . Furthermore, studies have shown that although NaF is a non-oxidant ion, it caused oxidative stress indirectly leading to DNA breakage 2,3 . Our results clearly demonstrated that NaF could not contribute to the damage of DNA.…”

Section: Discussionmentioning

confidence: 99%

Fluoride does not induce DNA breakage in Chinese hamster ovary cells in vitro

et al. 2004

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Fluoride has been widely used in dentistry because it is a specific and effective caries prophylactic agent. However, excess fluoride may represent a hazard to human health, especially by causing injury to genetic material. Genotoxicity tests represent an important part of cancer research to assess the risk of potential carcinogens. In the current study, the potential DNA damage associated with exposure to fluoride was assessed by the single cell gel (comet) assay in vitro. Chinese hamster ovary cells were exposed to sodium fluoride (NaF) at final concentration ranging from 7 to 100 µg/ml for 3 h, at 37°C. The results pointed out that NaF in all concentrations tested did not contribute to DNA damage as depicted by the mean tail moment and tail intensity. These findings are clinically important since they represent an important contribution to a correct evaluation of the potential health risk associated with the exposure to dental agents. DESCRIPTORS: Sodium fluoride; Comet assay; Mutagenicity tests. RESUMO:O flúor tem sido amplamente usado na Odontologia, pois é um agente profilático efetivo e específico contra a cárie dentária. Entretanto, o flúor em excesso pode representar perigos à saúde humana, especialmente por causar agressão ao material genético. Testes de genotoxicidade representam uma importante parte da pesquisa do câncer para a avaliação de risco de possíveis carcinógenos. Neste presente estudo, danos ao DNA associados à exposição ao flúor foram avaliados pelo teste de células individualizadas em gel de agarose (teste do cometa) in vitro. Células de ovário de hamster chinês foram expostas ao fluoreto de sódio (NaF) nas concentrações finais de 7 a 100 µg/ml, durante 3 h, a 37°C. Os resultados mostraram que o NaF não contribuiu para os danos no DNA em todas as concentrações testadas, conforme demonstrado pelas médias do momento da cauda e da intensidade da cauda dos cometas. Esses achados são clinicamente importantes, uma vez que representam uma importante contribuição para a correta avaliação do potencial risco à saúde associada à exposição aos agentes odontológicos. DESCRITORES: Fluoreto de sódio; Ensaio em cometa; Testes de mutagenicidade.

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“…Os membros anti-apoptóticos da família Bcl-2 inibem a apoptose impedindo a formação de poros na membrana mitocondrial e o extravasamento do citocromo c para o citosol (Gottlieb 2000). Caspases subsequentes são ativadas, culminando na clivagem de substratos específicos e na apoptose (Anuradha et al 2001).…”

Section: Introductionunclassified

Apoptose e maturação placentária bovina: um estudo imunohistoquímico e morfométrico

et al. 2016

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Placental release after birth involves loss of maternal-fetal adhesion and occurs only after complete maturation of the placentoma related to the decrease in cellularity of fetal and maternal tissues. Apoptosis is required for both the normal maturation and release of the placenta after birth. The aim of this study was to evaluate the occurrence of apoptosis in samples of the placenta of cows in different stages of gestation. Samples of 15 healthy cow placentomas at 4 (n=5), 6 (n=5) and 9 (n=5) months of gestation were harvested and processed for routine histology, immunohistochemistry and histochemistry. The slides were stained with HE, PicroSirius Red and subjected to immunohistochemical analysis of proteins Caspase 3, Caspase 8, Bax and Bid. Increase in number of vessels was not associated with increase in vascular area during progression of gestation. The results of histomorphometry revealed increased labeling for Bax and Caspases 3 and 8 in trophoblastic binucleated cells in late pregnancy, where the Bid remained without significant change. Histomorphometry analyzing the mononuclear trophoblast cells showed a high expression for Bax in early pregnancy, but decreased at 6 months of gestation. Immunolabeling revealed increased Caspases 3/8 and Bid with advancing of gestation. Further evaluation of type I and III collagen showed a decrease of both types of collagens at the end of gestation, what is very important for the reduction of maternal-fetal adhesion. These results confirm that Caspases 3 and 8 and Bax are involved in the mechanisms of activation of apoptosis through mitochondrial intrinsic and/or extrinsic pathway during pregnancy in trophoblastic binucleated cells. In mononuclear trophoblast cells Bax looses importance in the apoptosis process, awhile Bid and caspases 3 and 8 become the most significant.

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Oxidative damage to mitochondria is a preliminary step to caspase-3 activation in fluoride-induced apoptosis in HL-60 cells

Cited by 205 publications

References 42 publications

Camptothecin induced mitochondrial dysfunction leading to programmed cell death in unicellular hemoflagellate Leishmania donovani

Camptothecin induced mitochondrial dysfunction leading to programmed cell death in unicellular hemoflagellate Leishmania donovani

Fluoride does not induce DNA breakage in Chinese hamster ovary cells in vitro

Apoptose e maturação placentária bovina: um estudo imunohistoquímico e morfométrico

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