China
Africa
Explore chapters and articles related to this topic
#
Published in Sunil K. Deshmukh, Mandira Kochar, Pawan Kaur, Pushplata Prasad Singh, Nanotechnology in Agriculture and Environmental Science, 2023
Shweta Gehlout, Ayushi Priyam, Drishti, Luis Afonso, G Aaron Schultze, Pushplata Prasad Singh
NPs are believed to cause cytotoxicity of plant cells through pathways of apoptosis (programmed cell death) (Faisal et al., 2013; Ahmed et al., 2018). PCD is the genetically regulated process in multicellular eukaryotes which accounts for the elimination of undesirable and injured cells. In plants, PCD has a critical role in the control of developmental processes as well as environmental stress responses (Yamk et al., 2017). The three major forms of programmed cell death include apoptosis, autophagic cell death, and regulated necrosis (or necroptosis) (And6n and Faded’, 2013). Among the number of studies performed to correlate MNP exposure and PCD, one includes the study done for determining the effect of single-walled carbon nanotubes (SWCNTs) on rice plants (Oryza sativa subsp. japonica cv. Nipponbare), which showed the adverse effects of the NPs on protoplasts and leaves through induction of chromatin condensation and ROS accumulation as compared to control treatments in a dose-dependent manner (Shen et al., 2010).
Cellular Effects of Radio Frequency, Millimeter, and Terahertz Waves
Published in Ben Greenebaum, Frank Barnes, Biological and Medical Aspects of Electromagnetic Fields, 2018
Apoptosis, also called programmed cell death, is a defense mechanism that removes damaged cells, thereby maintaining the tissue, organ, or body in homeostasis. Cell death that occurs as a result of serious damage or being placed in an unfavorable cellular environment is called necrosis, which is distinct from apoptosis. Apoptosis, which occurs in response to DNA damage following exposure to chemical substances and IR, is a consequence of signal transduction via p53 or caspase-3. Two reports showed that RFW exposure has little effect on apoptosis (Hirose et al., 2006; Palumbo et al., 2008). However, several recent papers have reported that RFW exposure increases apoptosis due to reactive oxygen species mediated by caspase-3, as described below (Liu et al., 2012; Çiğ and Nazıroğlu, 2015). Although there is no consensus regarding the effects of RFW exposure on apoptosis, recent positive results are noteworthy and should be explored in future work.
Imaging of Cardiovascular Disease
Published in George C. Kagadis, Nancy L. Ford, Dimitrios N. Karnabatidis, George K. Loudos, Handbook of Small Animal Imaging, 2018
Aleksandra Kalinowska, Lawrence W. Dobrucki
In every living multicellular organism, programmed cell death is a naturally occurring and vital process, commonly termed as apoptosis. It allows the maintenance of homeostasis and the constant disposal of cells that are no longer needed. However, certain circumstances such as local hypoxia in sites of ischemia may lead to abnormal, increased apoptotic activity, which is a sign associated with many cardiovascular pathologies. As an example, it has been estimated that up to 30% of the injured myocardial tissue undergoes pathological apoptotic activity, making cell death markers an attractive target for molecular imaging. Apart from happening within the myocardium during MI, apoptosis is also associated with atherosclerotic plaque instability, congestive heart failure, and allograft rejection of the transplanted heart.
The effects of thymoquinone on DNA damage, apoptosis and oxidative stress in an osteoblast cell line exposed to ionizing radiation
Published in Radiation Effects and Defects in Solids, 2021
Osman Yılmaz, Veysel Yüksek, Sedat Çetin, Semiha Dede, Taylan Tuğrul
IR leads to cell death due to the damage it induces on the DNA. As a result of this, the functioning of the cellular metabolism is disrupted, and cellular ageing, different levels of molecular destruction and tissue and cell damage in organs most of which have vital significance occur (4,26). Apoptosis, which is also known as programmed cell death, involves highly complicated molecular cascade events. In whether or not a cell will go into apoptosis or necrosis, the types of various harmful stimulants such as radiation, temperature, hypoxia and drugs with cytotoxic effects are highly important. While the Caspase-3, Caspase-8 and Caspase-9 genes are proteins that are effective in the apoptotic pathway, it is known that the Bcl-2 gene is one of the apoptosis-regulating proteins (27). Moreover, the production and detoxification of free radicals that are formed as a result of IR are controlled with a highly sensitive balance. As long as the balance between the formation speed and elimination speed of these molecules is not disrupted, the cell is not affected by these procedures. When this balance is disrupted in cases where oxidants increase, or antioxidants fall short, oxidative stress occurs (4,26). It is also known that some antioxidant enzymes such as Gpx-3 and Sod-1 suppress this oxidative stress (28–30).
Role of the gene Phlda1 in fenvalerate-induced apoptosis and testicular damage in Sprague-Dawley rats
Published in Journal of Toxicology and Environmental Health, Part A, 2019
Ting Hong, Ru Li, Lu-Lu Sun, Jie Xu, Meng-Ting He, Wei Wang, Rui Yan, Jian Tong, Jie Zhang
Apoptosis, also termed programmed cell death, is an evolutionary conserved cell death process. It is now widely accepted that apoptosis is a genetically driven form of cell death where the balance of germ cell (GC) apoptosis and survival plays a critical role during normal development and homeostasis (Xu, Dong, and Yang 2016). The complicated mechanisms determining germ cell apoptosis may be divided into two main common pathways: the extrinsic pathway via death receptors and the intrinsic pathway via the mitochondria or endoplasmic reticulum (ER). It is of interest that Xu, Dong, and Yang (2016) reported that external adverse conditions such as exposure to environmental chemical exposures affect germ cell apoptosis. At present the role of apoptosis in the observed reproductive damage initiated by FEN an environmental contaminant is not known. The aim of this study was thus to determine whether cellular apoptosis was involved in FEN-induced testicular damage and whether it was possible to identify a genetic biomarker to predict of FEN-initiated damage.
Effects of astaxanthin on expression of apoptosis and oxidative stress related genes in H2O2 induced oxidative stress BE(2)-C human neuroblastoma cell line
Published in Preparative Biochemistry & Biotechnology, 2023
Maryam Hormozi, Nasim Beigi Boroujeni, Mandana Beigi Boroujeni
Apoptosis is a programmed cell death which can be physiological or pathological. This process is controlled by apoptosis-inducing molecules such as Bax, Caspases, P53 and apoptosis-inhibitory molecules such as Bcl2.[1] Like other biological molecules, these molecules are encoded by their genes, and therefore, gene expression study is common to investigate apoptosis. There are some triggers of apoptosis that one of them is oxidative stress.[2] Hence, in the cases of pathologic apoptosis induced by oxidative agents, we are trying to inhibit apoptosis by some interventions like using antioxidants.[3] Briefly, apoptosis is a common outcome variable in biological researches.