DNA adducts-chemical addons

Rajalakshmi, T. R.; AravindhaBabu, N; Shanmugam, K. T.; Masthan, K. M. K.

doi:10.4103/0975-7406.155901

Cited by 21 publications

(13 citation statements)

References 8 publications

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“…Nucleophilic targets of the reactive carcinogen include nitrogen and oxygen atoms within the bases and phosphodiester backbone of DNA. The binding of the electrophile to a nucleophile is dependent on the electrophilic strength of the carcinogen [ 56 – 58 ]. Common target sites on DNA include N and O of guanine or N of adenine [ 56 ] (see Table 1 ).…”

Section: Chemical-induced Bulky Dna Lesionsmentioning

confidence: 99%

Carcinogens and DNA damage

Barnes

Zubair

John

et al. 2018

Biochemical Society Transactions

231

126

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Humans are variously and continuously exposed to a wide range of different DNA-damaging agents, some of which are classed as carcinogens. DNA damage can arise from exposure to exogenous agents, but damage from endogenous processes is probably far more prevalent. That said, epidemiological studies of migrant populations from regions of low cancer risk to high cancer risk countries point to a role for environmental and/or lifestyle factors playing a pivotal part in cancer aetiology. One might reasonably surmise from this that carcinogens found in our environment or diet are culpable. Exposure to carcinogens is associated with various forms of DNA damage such as single-stand breaks, double-strand breaks, covalently bound chemical DNA adducts, oxidative-induced lesions and DNA–DNA or DNA–protein cross-links. This review predominantly concentrates on DNA damage induced by the following carcinogens: polycyclic aromatic hydrocarbons, heterocyclic aromatic amines, mycotoxins, ultraviolet light, ionising radiation, aristolochic acid, nitrosamines and particulate matter. Additionally, we allude to some of the cancer types where there is molecular epidemiological evidence that these agents are aetiological risk factors. The complex role that carcinogens play in the pathophysiology of cancer development remains obscure, but DNA damage remains pivotal to this process.

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Section: Chemical-induced Bulky Dna Lesionsmentioning

confidence: 99%

Carcinogens and DNA damage

Barnes

Zubair

John

et al. 2018

Biochemical Society Transactions

231

126

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“…Metoprolol has the cytotoxic activity in testes which is responsible for the low sperm count(9) and sperm viability. DNA adducts was formed by many drugs especially cisplatin and oxaliplatin (10,11) preventing DNA repair and has negative effect on genome integrity of cancer cells. In present study Metoprolol is able to form DNA adducts which give absorption maxima at 265-270nm.The DNA used is Pure as digestion with DNase resulted in loss of peak and appearance of absorption maxima at 223-226 nm which is metosartan.…”

Section: Discussionmentioning

confidence: 99%

Dual Role of RNase A and Metosartan: An Examination in invitro & invivo Condition

Beeram

2019

NN-PBS

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Metosartan consists of two components Metoprolol and telmisartan. Telmisartan inhibits RNase A in rat testes by uncompetitive inhibition where as Metoprolol forms DNA adducts and reduces sperm count. Metosartan decreases testes viability and sperm count was found to be high in metosartan treated rats compared to Metosartan +RNase A group. RNase A induces Netosis in both invivo and invitro condition in both RNase treated group and as well as RNase A+ Metosartan. Deep cold storage of mitochondria induces expression of cyt P450gene in testes mitochondria but not in sperm.

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“… 134 , 135 , 136 DNA adducts are sections of the DNA strand that are covalently bound to chemical compounds, which cause abnormalities during DNA replication that can lead to genetic mutations. 137 …”

Section: Evidence Linking Periodontitis and Several Types Of Cancermentioning

confidence: 99%

Paradigm shift in the pathogenesis and treatment of oral cancer and other cancers focused on the oralome and antimicrobial‐based therapeutics

Radaic

Ganther

Kamarajan

et al. 2021

Periodontology 2000

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The oral cavity contains up to 1000 microbial species in total, comprised of bacteria, fungi, viral, archaea, and protozoan species that thrive in a very dynamic microenviroment. [1][2][3][4][5] All of these microorganisms form a complex relationship among themselves, establishing a unique microbiome, known as the oral microbiome. Interestingly, the oral microbiome forms a close symbiotic relationship with human host cells in the oral cavity. Thus, the term oralome was coined to encompass not only the oral microbiome but also the host-microbial interactions that take place in the human oral cavity. 5 In this sense, healthy symbiotic host-microbiome interactions between humans and these microorganisms are known as eubiosis. [5][6][7] The microbial composition can be dramatically affected by interspecies and host-microbial interactions. These microbial changes can impact the health and disease status of the host, since eubiosis plays an essential role both in the development of natural oral physiology and host defense mechanisms. 5,8,9 Although the oral microbiome can compensate for most overall perturbations, 5,10 some changes can profoundly affect its composition, impacting the oral commensal populations and causing an unbalanced state known as dysbiosis. 5,11 | Periodontitis and oral microbiome dysbiosisDysbiosis is an unbalanced microbiome state that is caused by internal and/or external microbial-ecologic changes to the oral microbiome. 5 This specific state has been described as capable of promoting diseases in the host. 12,13 Since periodontitis is considered an inflammatory disease that is initiated by pathogenic bacteria, the most accepted hypothesis for periodontitis initiation and progression is that there is a dysbiotic shift in the oral microbiome. 5,14 This shift is driven by an enrichment of Prevotella intermedia, Fusobacterium nucleatum, Porphyromonas gingivalis, Tannarella forsythia, and Treponema denticola species in the microbiome. [14][15][16] Specifically, a dysbiotic oral biofilm infiltrates the gingival pocket, which then triggers the host immune response. This reaction leads to gingival tissue inflammation (gingivitis) and, ultimately, tissue degradation and periodontitis. 14 Oral dysbiosis has been associated with a variety of systemic diseases and conditions, including Alzheimer's disease, diabetes, adverse pregnancy complications, and several types of cancer, including oral, gastrointestinal, lung, breast, prostate, and uterine cancer. 5,[17][18][19][20] Thus, the objective of this research is to (1) evaluate the epidemiologic evidence linking periodontitis to these types of cancer, (2) provide insights into the mechanisms by which oral microbial dysbiosis can cause these cancers, and (3) summarize the evolving evidence supporting the use of probiotics and related moleculesThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use...

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DNA adducts-chemical addons

Cited by 21 publications

References 8 publications

Carcinogens and DNA damage

Carcinogens and DNA damage

Dual Role of RNase A and Metosartan: An Examination in invitro & invivo Condition

Paradigm shift in the pathogenesis and treatment of oral cancer and other cancers focused on the oralome and antimicrobial‐based therapeutics

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