In recent decades, metal oxide nanoparticles have acquired relevance in biology and medicine due to their unique physicochemical properties. Because of its cheap cost, biodegradability and low toxicity, zinc oxide nanoparticles (ZnO-NPs) have attracted a lot of interest from researchers for therapeutic and diagnostic applications. Zinc oxide (ZnO) has been studied for various biological applications due to its unique semiconducting, optical and piezoelectric characteristics. The growing interest in nano zinc oxide has led to the discovery and development of nanoparticle production technologies. ZnO nanocomposites with varied morphologies have recently been prepared using a physical and chemical method. ZnO NPs have also been employed to deliver different bioactive and chemotherapeutic anticancer medicines to tumour cells in a targeted and sustained manner. This review discusses on the properties, synthesis, drug delivery method for cancer treatment and many other biological uses of ZnO NPs.
Several cell death modes, each with a unique feature and mode of inducing cell death have been established. Cell death occurring under physiological conditions is primarily caused by apoptosis, which is a non-inflammatory or silent process, whereas necroptosis or pyroptosis is triggered by pathogen invasion, which stimulates the immune system and induces inflammation. In physiology, clearing dead cells and associated cellular debris is necessary since billions of cells die during mammalian embryogenesis and every day in adult organisms. For degradation, dead cells produced by apoptosis are quickly engulfed by macrophages. This chapter will present a description of the phagocytosis of dead and dying cells, by a process known as efferocytosis. Macrophages and, to a lesser degree, other ‘professional’ phagocytes (such as monocytes and dendritic cells) and ‘non-professional’ phagocytes, such as epithelial cells, conduct efferocytosis. Recent discoveries have shed light on this mechanism and how it works to preserve homeostasis of tissue, repair of tissue and health of the organism. Caspases are a large family of proteases of cysteine acting in cascades. A cascade leading to activation of caspase 3 mediates apoptosis and is responsible for killing cells, hiring macrophages, and presenting a “eat me” signal(s). If macrophages do not effectively engulf apoptotic cells, they undergo secondary necrosis and release intracellular materials that reflect a molecular pattern associated with injury, which can lead to autoimmune diseases. Here, the processes of efferocytosis are illustrated and the pathophysiological effects that which occur when this phase is abrogated are highlighted.
It has been discovered that bisphenol A (BPA), an established anthropogenic xenoestrogen, is a causal factor in developing cancer, cognitive impairment, neurotoxicity, oxidative stress, and other harmful effects in humans and other species. Although there is some research into the mechanisms of BPA-induced toxicity, it is unclear whether there is a chance of amelioration through natural intervention. Zebrafish (Danio rerio) were used in this study after waterborne exposure to BPA, to assess whether carvacrol co-supplementation could reduce the destructive potential of the compound. All the chemicals and reagents utilized in the current investigations were purchased from Sigma-Aldrich, Ottochem, India. 5-7month-old zebrafish were acquired from a local fish store in Kolathur, Chennai and kept in a 50-L tank at a constant temperature of 25±2ºC. There were no animal ethical issues involved to carry out this research. Laboratory studies were conducted to determine whether the antioxidant nature of carvacrol might protect the zebrafish brain from BPA-induced altered behavioural responses and oxidative stress. The current data demonstrates that carvacrol is effective in alleviating the altered behavioural response caused by BPA. Biochemical investigations in the zebrafish brain suggest that carvacrol may have therapeutic potential in treating oxidative stress induced by BPA. In addition, the zebrafish brain is protected by carvacrol against BPA-induced toxicity. These preliminary data suggest that carvacrol may be a helpful intervention in treating BPA-induced toxicity in zebrafish by inhibiting the reactive oxygen species production. Novel therapeutic approaches for treating BPA-induced predisposition to severe illnesses could emerge from future research on signaling cascades.
The man-made xenoestrogen bisphenol S has been well-established and associated with developing neoplasm, dementia, neurotoxicity, anxiety, and other adverse effects in people and other organisms. The mechanisms of BPS-induced toxicity have been studied; however, it is unclear if there is any prospect for improvement by natural means. After being exposed to BPS through water, zebrafish (Danio rerio) were employed in this investigation to determine whether quercetin co-supplementation could lessen the compound's destructive potential. Laboratory tests were done to see if quercetin's antioxidant properties may shield the zebrafish brain from oxidative stress and altered behavioral responses brought on by BPS. The available evidence shows that quercetin is beneficial in reducing the abnormal behavioral response brought on by BPS. Quercetin (QU) may have therapeutic potential for reducing oxidative stress caused by BPS, according to biochemical research conducted in the zebrafish brain. In addition, quercetin guards the zebrafish brain against toxicity brought on by BPS. These preliminary findings imply that quercetin, which reduces the generation of reactive oxygen species, would be an effective treatment for BPS-induced toxicity in zebrafish.
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