Background: Increasing antimicrobial resistance (AMR) raises serious health and financial concerns. However, the main drivers of the emergence, spread and subsequent colonisation of resistant bacterial strains between humans, animals and the environment are still poorly understood.Objective: The aim of this review was to identify molecular studies on AMR in One Health settings in Africa and to determine the prevalence of antimicrobial resistance genes in humans, animals and the environment. Due to the very low number of studies including environmental samples, the meta-analysis only includes data obtained from animals and humans. Methods:The PubMed, Web of Science and Scopus databases were searched, identifying 10 464 publications on AMR in Africa from January 1st, 2000 until June 1st, 2020. Inclusion criteria were: (i) Integrated studies assessing AMR simultaneously in an animal-human, animal-environment, human-environment or animal-humanenvironment context, (ii) Genotypic characterisation of AMR and (iii) temporal and spatial relationship between samples from humans and animals. Statistical randomeffects model meta-analysis was performed. Results:Overall, 18 studies met our eligibility criteria and were included in this review.Six studies investigated Escherichia coli and Salmonella spp. (N = 6). The most prevalent AMR genes in animals included sul1 (36.2%), sul2 (32.0%), tetA (31.5%), strB (30.8%) and blaTEM (30.0%), whereas sul2 (42.4%), tetA (42.0%), strB (34.9%), blaTEM (28.8%) and sul1 (27.8%) were most prevalent in humans. We observed no clear pattern for a higher prevalence in either the animal or the human reservoir. Conclusion:To date, data on AMR in a One Health perspective in Africa are scarce.Prospective and longitudinal studies using an integrated One Health approach assessing the environment, animals and humans at the same time are needed to better understand the main drivers of AMR sharing in Africa.
The O 6-alkylguanosine adduct O 6-carboxymethyldeoxyguanosine (O 6-CMdG) has been detected at elevated levels in blood and tissue samples from colorectal cancer patients and from healthy volunteers after consuming red meat. The diazo compound l-azaserine leads to the formation of O 6-CMdG as well as the corresponding methyl adduct O 6-methyldeoxyguanosine (O 6-MedG) in cells and is therefore in wide use as a chemical probe in cellular studies concerning DNA damage and mutation. However, there remain knowledge gaps concerning the chemical basis of DNA adduct formation by l-azaserine. To characterize O 6-CMdG formation by l-azaserine, we carried out a combination of chemical and enzymatic stability and reactivity studies supported by liquid chromatography tandem mass spectrometry for the simultaneous quantification of O 6-CMdG and O 6-MedG. We found that l-azaserine is stable under physiological and alkaline conditions as well as in active biological matrices but undergoes acid-catalyzed hydrolysis. We show, for the first time, that l-azaserine reacts directly with guanosine (dG) and oligonucleotides to form an O 6-serine-CMdG (O 6-Ser-CMdG) adduct. Moreover, by characterizing the reaction of dG with l-azaserine, we demonstrate that O 6-Ser-CMdG forms as an intermediate that spontaneously decomposes to form O 6-CMdG. Finally, we quantified levels of O 6-CMdG and O 6-MedG in a human cell line exposed to l-azaserine and found maximal adduct levels after 48 h. The findings of this work elucidate the chemical basis of how l-azaserine reacts with deoxyguanosine and support its use as a chemical probe for N-nitroso compound exposure in carcinogenesis research, particularly concerning the identification of pathways and factors that promote adduct formation.
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