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Nanomaterials in Cardio Protection
Published in Parimelazhagan Thangaraj, Lucindo José Quintans Júnior, Nagamony Ponpandian, Nanophytomedicine, 2023
The characteristic events in ischemia are typically when a blockage occurs in the blood flow followed by reperfusion, which attempts to re-establish blood flow to the affected area. Ironically, reperfusion of blood causes reperfusion-induced cell death, leading ischemia reperfusion (IR) injury, a key topic to address. Fundamental events that are addressed in cardiac research are oxidative stress, calcium overload and intracellular acidosis inducing the opening of the mitochondrial permeability transition pore (mPTP) (Hausenloy and Yellon 2013). This causes the release of cytochrome C to the cytosol and activates the caspases, causing apoptosis. Downstream inflammatory responses include recruitment of neutrophils, monocytes and macrophages. Disease conditions, specifically acute myocardial infarction (AMI), are bound to experience IR injury. Alleviating any of these conditions would then be termed cardio protection.
Cell Biology for Bioprocessing
Published in Wei-Shou Hu, Cell Culture Bioprocess Engineering, 2020
In addition to their role in energy metabolism, mitochondria also play a key role in the regulation of apoptosis. Some pro-apoptotic proteins are sequestered in the space between the outer and inner membranes of mitochondria. Cytochrome C, a hemeprotein that is an important component of the cytochrome C complex in the electron transport chain, is associated with the inner membrane of mitochondria. The release of cytochrome C and those pro-apoptotic proteins in stressed cells initiates the intrinsic pathway of apoptosis (Figure 2.22). The cytochrome C released into the cytoplasm proceeds to form a complex with APF1, pro-caspase 9, and dATP, known collectively as the apoptosome. In the apoptosome, the inactive pro-caspase 9 becomes activated and subsequently activates downstream caspases.
Applications
Published in Raj P. Chhabra, CRC Handbook of Thermal Engineering Second Edition, 2017
Joshua D. Ramsey, Ken Bell, Ramesh K. Shah, Bengt Sundén, Zan Wu, Clement Kleinstreuer, Zelin Xu, D. Ian Wilson, Graham T. Polley, John A. Pearce, Kenneth R. Diller, Jonathan W. Valvano, David W. Yarbrough, Moncef Krarti, John Zhai, Jan Kośny, Christian K. Bach, Ian H. Bell, Craig R. Bradshaw, Eckhard A. Groll, Abhinav Krishna, Orkan Kurtulus, Margaret M. Mathison, Bryce Shaffer, Bin Yang, Xinye Zhang, Davide Ziviani, Robert F. Boehm, Anthony F. Mills, Santanu Bandyopadhyay, Shankar Narasimhan, Donald L. Fenton, Raj M. Manglik, Sameer Khandekar, Mario F. Trujillo, Rolf D. Reitz, Milind A. Jog, Prabhat Kumar, K.P. Sandeep, Sanjiv Sinha, Krishna Valavala, Jun Ma, Pradeep Lall, Harold R. Jacobs, Mangesh Chaudhari, Amit Agrawal, Robert J. Moffat, Tadhg O’Donovan, Jungho Kim, S.A. Sherif, Alan T. McDonald, Arturo Pacheco-Vega, Gerardo Diaz, Mihir Sen, K.T. Yang, Martine Rueff, Evelyne Mauret, Pawel Wawrzyniak, Ireneusz Zbicinski, Mariia Sobulska, P.S. Ghoshdastidar, Naveen Tiwari, Rajappa Tadepalli, Raj Ganesh S. Pala, Desh Bandhu Singh, G. N. Tiwari
In Eissing’s biochemical model, the initiator (i.e., input signal) caspases (C2, C8, C9, C10, etc.) are represented by activated caspase 8, C8*. There are, of course, many other input signals; for example p52, the “guardian of the genome” and death receptors like FADD (Fas-associated death domain).129 The executioner caspases (C3, C6, C7, etc.) are represented by activated caspase 3, C3*. Caspase 9 has somewhat of a dual role in that in addition to signaling it participates as the hub of an “apoptosome”, a large flower-shaped molecule, with the protein APAF1 forming “petals” tipped with cytochrome C.99,129 There is also intimate coupling between apoptosis and metabolism.138 Cytochrome C, in turn, is a critical participant in the final stages of oxidative phosphorylation on the outer leaflet of the inner membrane of mitochondria, where it is responsible for electron transport between complexes III and IV, immediately upstream of ATP synthase, the final step.99,129 Presumably, cytochrome C plays a similar role at the tips of the apoptosome petals.
A review of quorum sensing regulating heavy metal resistance in anammox process: Relations, mechanisms and prospects
Published in Critical Reviews in Environmental Science and Technology, 2023
Caiyan Qu, Fan Feng, Jia Tang, Xi Tang, Di Wu, Ruiyang Xiao, Xiaobo Min, Chong-Jian Tang
QS enhances the synthesis of electron shuttles to mediate the electron transfer during the redox transformation of heavy metals. The cytochrome c protein containing heme c approximately accounts for 20% of the cellular proteins in anammox cells, which participates in electron transfer of anammox respiratory chain (Wang & Zheng, 2017; Feng et al., 2022). AHL addition significantly upregulated the expression of genes encoding cytochrome P450 and cytochrome c precursor, resulting in an increased production of these cytochrome. The cytochrome facilitated the electron transfer from intracellular ubiquinone to the cytoplasmic space (Whiteley et al., 1999). Additionally, AHL increased the NAD level of anammox consortia in the metabolite analysis, suggesting that AHL-mediated QS could increase the amount of electron shuttles (Tang et al., 2018b). Subsequently, cytochrome c and NADH (the reduction state of NAD) were reported to catalyze V(V) and Cr(VI) reduction to V(IV) and Cr(III), respectively (Shi et al., 2020).
Evaluation of in vitro cytotoxicity and in vivo potential toxicity of the extract from in vitro cultivated Anoectochilus roxburghii Lindl
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Doan Chinh Chung, Thanh Long Le, Nguyen Quynh Chi Ho, Thi Thuy Nguyen, Dang Giap Do, Duc Thang Do, Thi Phuong Mai Nguyen, Thi Phuong Thao Nguyen, Nghia Son Hoang
Cytochrome c is released from mitochondria into cytosol where it activates the caspase cascade for apoptotic cell death. Thus, to determine whether caspase activation is related to intrinsic apoptosis, the mRNA and protein expression levels of caspase-3, caspase-9, and PARP were measured. As illustrated in Figure 5, a marked rise in mRNA and protein expression levels of caspase-3 was observed in iARE-treated cells. At a concentration of 100 µg/ml iARE stimulated a significant elevation of mRNA and protein expression levels of caspase-3 up to 2.85 – and 1.92-fold, respectively, in comparison with control. Similarly, the mRNA and protein expression levels of caspase-9 displayed a significant increase at the mRNA level but a numerical increment at protein level in iARE-exposed MCF7 cells compared to the control. Further, mRNA and protein PARP expression levels were reduced and a cleavage of PARP into fragments occurred in iARE-treated cells (Figure 5). These results were similar to those observed in VP16-treated cells.
27-Deoxyactein prevents 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced cellular damage in MC3T3-E1 osteoblastic cells
Published in Journal of Environmental Science and Health, Part A, 2018
Kwang Sik Suh, Eun Mi Choi, Woon-Won Jung, So Young Park, Sang Ouk Chin, Sang Youl Rhee, Youngmi Kim Pak, Suk Chon
Cardiolipin oxidation induces the opening of permeability pores in the outer mitochondrial membrane, which permits the release of cytochrome c and other pro-apoptotic factors from the mitochondria into the cytosol. Subsequently, cytochrome c release triggers a cascade of caspase interactions that leads to apoptosis.[35] Cardiolipin exists in association with cytochrome c on the outer surface of the inner mitochondrial membrane. Thus, to obtain further evidence of oxidative stress within the mitochondria, the oxidation of cardiolipin was assessed. Because the fluorescent dye NAO binds to the non-oxidized form but not the oxidized form of cardiolipin,[36] measurements of NAO fluorescence allow for the monitoring of the oxidation of cardiolipin in mitochondria. In the present study, treatment with 100 nM of TCDD decreased NAO fluorescence, indicating that cardiolipin peroxidation was induced (Fig. 5). However, 27-deoxyactein (0.01–1 μM) reduced the level of TCDD-induced cardiolipin peroxidation, which suggests that 27-deoxyactein reduced ROS generation and oxidative stress within the mitochondria that were induced by TCDD.