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Genetic toxicology
Published in Chris Winder, Neill Stacey, Occupational Toxicology, 2004
They occur in approximately 0.6% of live births in humans. It has been estimated that up to 40% of spontaneous abortuses have chromosomal defects. The rationale for measuring chromosomal effects includes: the increasing evidence that specific chromosomal defects in somatic cells are associated with most neoplasias and evidence that chromosomal rearrangement may play a role in oncogene activation; the relevance of chromosomal mutation to inheritance of genetic defects in germ cells; and the observation that substances which produce chromosomal structural changes also produce point mutations and that few gene mutagens produce no aberrations.
Chemical Carcinogenesis in Skin: Causation, Mechanism, and Role of Oncogenes
Published in Rhoda G. M. Wang, James B. Knaak, Howard I. Maibach, Health Risk Assessment, 2017
The concept of DNA binding as an essential step in chemical carcinogenesis has recently gained considerable support from studies on oncogenes,74,75 initially identified as the transforming genetic constituents of certain RNA tumor viruses. In general, viral oncogenes closely resemble the genes of eukaryotic cells, known as protooncogenes. At least 50 different protooncogenes are known, which code for proteins required for the reception, transduction, and interpretation of endogenous mitogenic signals such as growth factors. The biochemical route of the “mitotic cascade” governed by protooncogene products may play a key role in embryonic development, tissue regeneration, and wound repair.74-76 Neoplastic transformations may be related to inappropriate expression of protooncogenes as a result of chromosomal rearrangement, gene amplification, point mutation, or other genetic alterations.77,78 Of various cellular protooncogenes studied, the Ha-ras gene has been found to be activated in several spontaneous and induced malignant neoplasms.79 The ras family of protooncogenes was first discovered as oncogenes contained in Harvey and Kirsten rat sarcoma viruses80 and forms a family of at least three genes81-83 which are altered in about 10 to 20% of most human tumors.84 The cHa-, cKi-, and cN-ras genes encode for very similar p21 proteins of 188 to 189 amino acids.85 The positions at which single amino acid substitution can lead to transforming activity86 include amino acids 12, 13, 59, 61, and 63. Of these, mutations at three sites have been identified in human and mouse tumors.87-89 As reported by Barbacid,90 chemically induced mouse and human skin carcinomas and other epithelial tumors contain activated cHa-ras.
Plant mediated synthesis of AgNPs and its applications: an overview
Published in Inorganic and Nano-Metal Chemistry, 2021
Aswathi Shyam, Smitha Chandran S., Bini George, Sreelekha E.
While dealing with nanoparticles inside the human cells, it is important to understand the toxicity levels of AgNPs also. Even though the AgNPs are widely acceptable for cancer treatment and wound dressing, through which it can easily enter the human cells, only a few studies are done on toxicity of AgNP. The same mechanism of toxicity that is applicable to microorganism can be active for human also. NPs exhibit an enhanced in vivo deed due to its larger surface area and small size. A study on the effect of AgNPs on ATP production, cell cycle, cell viability, DNA damage, and chromosomal aberrations is carried out by P.V. Asharani et al. using starch coated AgNP. The most noticeable change on cells due to NP treatment is the alteration in cell morphology or shape. Cells that are treated with NPs appear in clusters with small extensions because of the interference in cytoskeletal functions. ATP assays showed that even after 24 h of incubation content of the cell was not affected significantly. But after 48 h, the ATP content dropped drastically and continued for next 72 h indicating a metabolic arrest that can be taken as a symbol of ATP depletion and cytotoxicity. The electron transport chain was disturbed by malfunctioning of mitochondria that arised due to the Ag-NP deposition. Reactive oxygen species formation and low ATP yield is the result of this. Since ROS are highly reactive it may cause oxidative damage to DNA and protein. After cell treatment with AgNP, DNA experience extensive, and dose dependent damage, that may result in chromosome rearrangement. With the increase in NP concentration, increase in DNA damage was observed in cancer cells.[87]