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Understanding the Interaction of Nanoparticles at the Cellular Interface
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
A cell is a fundamental unit of life bestowed with vivid cell organelles for controlling unique functions. For instance, their roles in cell repair, waste removal, and growth give them the privilege to tasks as a mini-organ. In these contexts, intracellular interaction of NPs, after a successful internalization process, plays a pivotal role in various therapeutic strategies against multiple diseases such as cancer. Tuning and taming these organelles’ extraordinary properties using nanomaterials can revolutionize the treatment strategy against most of the conditions of the prevailing disease by providing sufficient dosage, controlled release, and address the limitation of drug resistance. So far, the mitochondria, Golgi apparatus, and nucleus are the most explored cell organelle for the direct nanoparticle interactions to check the cytotoxicity activities (Figure 2.4).
Tropical Herbs and Spices as Functional Foods with Antidiabetic Activities
Published in Megh R. Goyal, Arijit Nath, Rasul Hafiz Ansar Suleria, Plant-Based Functional Foods and Phytochemicals, 2021
Arnia Sari Mukaromah, Fitria Susilowati
Apigenin and luteolin act as Sodium-glucose Cotransporter-2 (SGLT-2) inhibitors in neuropathic diabetes [39]. Several scientific facts indicate that oxidative stress affects DM pathogenesis and diabetic complications. The elaboration of glucose oxidation, glycation of proteins, and oxidative deterioration of proteins can lead to the formation and accumulation of free radicals in DM patients. This peculiarity of free radicals and chronic deterioration in endogenous antioxidants cause harm to cell organelles and oxidative enzymes [57].
Finding a Target
Published in Nathan Keighley, Miraculous Medicines and the Chemistry of Drug Design, 2020
The instructions for producing proteins are encoded on genes, sections of DNA, which are transcribed on to RNA before being translated into a protein chain at ribosomes; cell organelles designed for this operation. This is a very intricate enzyme-controlled biological pathway, with a high degree of complexity. Proteins produced from this process then adopt their specific three-dimensional shape and move to their intended location to perform a given function in the body. Nucleotide triplets code for particular amino acids; the order in which these triplets are assembled in the gene determines the sequence of amino acids in the protein and therefore ultimately governs the proteins shape and function. The different side chains of each of the 20 amino acids can form a variety of hydrogen bonds; hence the observed variety of possible structures. Proteins are very versatile molecules that can have many functions, governed by their structural organisation. For globular proteins such as those involved in catalysis and molecular recognition, the final folded three-dimensional shape of a polypeptide, the tertiary structure, may constitute one protein domain, and several globular units comprise the functional quaternary structure, as with haemoglobin. In order for polypeptides to assemble into a functioning quaternary structure, precise interactions between these molecules must be in place.
Identification of Rab7 as an autophagy marker: potential therapeutic approaches and the effect of Qi Teng Xiao Zhuo granule in chronic glomerulonephritis
Published in Pharmaceutical Biology, 2023
Xiujuan Qin, Huiyu Chen, Xiaoli Zhu, Xianjin Xu, Jiarong Gao
Mitochondria are important eukaryotic cell organelles; they produce ATP via oxidative phosphorylation and provide 95% of the cell’s energy requirements. They are also involved in metabolic signal transduction, inflammation, and apoptosis regulation. The kidney is rich in mitochondria, which play a key role in its function, and mitochondrial damage and dysfunction are major factors in many chronic and acute kidney diseases (Tang et al. 2021). Maintaining mitochondrial homeostasis and metabolic balance is crucial for kidney function (Bhargava and Schnellmann 2017). When mitochondrial damage and dysfunction occur, mitophagy is induced to maintain cell homeostasis, removing damaged or excess mitochondria (Su et al. 2023). Transmission electron microscopy showed that abnormal mitochondrial cristae and decreased autophagosomes were apparent in the model group. Interestingly, we also found that mitochondrial damage was reduced after QTXZG treatment.
Platelet-derived mitochondria transfer facilitates wound-closure by modulating ROS levels in dermal fibroblasts
Published in Platelets, 2023
Soomin Kim, Yujin Kim, Shin-Hye Yu, Seo-Eun Lee, Jong Hyeok Park, Gayoung Cho, Chul Choi, Kyuboem Han, Chun-Hyung Kim, Young Cheol Kang
Mitochondria are cell organelles important for cellular functions by providing energy in the form of ATP through oxidative phosphorylation, in which ROS are generated as by-products [6]. Mitochondria also play critical roles in apoptosis, inflammation, and calcium homeostasis. Given their important roles in cellular physiology, mitochondrial dysfunction can result in impaired bioenergetic efficiency, which in turn leads to abnormal inflammatory responses and excessive ROS. Recently, application of mitochondria isolated from healthy cells (referred to as mitochondria transfer) has become an attractive therapeutic strategy for treating mitochondrial abnormalities [7–10]. The aim of mitochondrial transfer is to replace intracellular abnormal mitochondria with healthy mitochondria isolated from normal cells, resulting in the recovery of cell function. Therefore, transfer of healthy mitochondria into cells with damaged mitochondria could be beneficial to restore excessive ROS production and mitochondrial dysfunction.
Diabetic cardiomyopathy attenuated the protective effect of ischaemic post-conditioning against ischaemia-reperfusion injury in the isolated rat heart model
Published in Archives of Physiology and Biochemistry, 2023
Gino A. Kurian, Mahalakshmi Ansari, Priyanka N. Prem
Oxidative stress was evaluated by measuring the activities of enzymatic antioxidants viz., SOD, catalase, GPx, GR and concentration of non-enzymatic antioxidant like GSH along with the level of free radical-induced lipid peroxidation product, MDA (malondialdehyde) and the results are shown in Figure 3. MDA and glutathione concentration (one of the major antioxidant in heart) in tissue and cell organelle is considered as a major index to evaluate oxidative stress. Accordingly, at the basal level determination, both DM and DCM heart displayed a significant rise in MDA level and corresponding decline in GSH level with reduced activities of antioxidant enzymes, compared to the normal heart, confirming the severe oxidative stress at the baseline level. However, upon reperfusion, these hearts were not showed any prominent change as that of normal (Figure 3), and the same was observed in POC procedure as well. In addition, we evaluated oxidative status in sub-cellular level, which includes mitochondria and microsomal fractions and the results are shown in Figure 4 and Supplementary Figure 4. In mitochondrial fraction, both DM and DCM heart displayed higher MDA level (SSM and IFM) and declined GSH level (SSM and IFM) at the baseline level evaluation. Further increase in MDA and decrease in GSH was observed with I/R treated DCM rat heart, with no change in DM heart (Figure 4). However, POC procedure failed to limit oxidative stress in both DM and DCM heart.