November 10, 2024

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Gut Bacteria’s Role in Amplifying Carcinogen Intake Leads to Distant Tumors

Gut Bacteria’s Role in Amplifying Carcinogen Intake Leads to Distant Tumors



Gut Bacteria’s Role in Amplifying Carcinogen Intake Leads to Distant Tumors

On July 31, a paper published in Nature titled “Gut Microbiota Carcinogen Metabolism Causes Distal Tissue Tumours” revealed groundbreaking findings.

The research, conducted by a team from the European Molecular Biology Laboratory (EMBL) in Heidelberg, Germany, and the University of Split in Croatia, highlights that the metabolism and biotransformation of a common tobacco carcinogen, nitrosamine, within the human body are significantly influenced by gut microbiota. Variations in the gut microbiota composition among individuals determine the rate at which nitrosamine metabolites accumulate in the bladder and ultimately whether they cause bladder cancer.

Gut Bacteria's Role in Amplifying Carcinogen Intake Leads to Distant Tumors

For many years, laboratories worldwide have induced bladder cancer in mice using nitrosamine (BBN) to establish cancer models. However, the Croatian researchers saw potential in this classic method to explore how the gut microbiome’s metabolic environment affects the subsequent carcinogenic effects of carcinogens. This led them to a surprising discovery: when antibiotics were added to the drinking water of mice, effectively eliminating gut microbiota, only 19% of the mice exhibited pathological changes in the bladder indicative of cancer after 12 weeks. This is in stark contrast to the control group, where 77% of the mice developed bladder cancer, underscoring the critical influence of gut microbiota.

With these results in hand, Croatian researcher Professor Janoš Terzić collaborated with renowned EMBL expert Michael Zimmermann. Using EMBL’s advanced laboratory facilities, they confirmed that in antibiotic-treated, nitrosamine-induced mouse models, the levels of nitrosamine metabolite BCPN were significantly reduced, and more BCPN was excreted via urine. This reduction in BCPN levels was key to the lower incidence of bladder cancer in these mice.

The researchers traced the metabolic pathway of nitrosamine to BCPN in mice, confirming that nitrosamine is oxidatively metabolized to BCPN and its derivatives in the colon. These metabolites then accumulate in the bladder, promoting cancer development, a process dependent on the presence of gut microbiota. Antibiotic treatment disrupts this process.

Further analysis identified 12 gut microbiota species (from eight different genera) involved in the metabolic process, including Escherichia and Pseudolabrys. Analysis of human fecal samples showed that these nitrosamine-metabolizing microbes are also present in humans, although their abundance varies significantly between individuals.

Due to individual differences in gut microbiota composition, the rate of nitrosamine metabolism varies widely among people. This means that even with similar nitrosamine intake, the levels of BCPN and the speed at which it accumulates in the bladder differ, potentially explaining individual differences in bladder cancer risk.

Could similar phenomena occur with other environmental carcinogens in the human body? This question opens a new and promising research direction for cancer prevention and treatment by targeting gut microbiota.

Gut Bacteria’s Role in Amplifying Carcinogen Intake Leads to Distant Tumors


References:

[1]Roje B, Zhang B, Mastrorilli E, et al. Gut microbiota carcinogen metabolism causes distal tissue tumours[J]. Nature, 2024.

[2]https://www.sciencedaily.com/releases/2024/07/240731140914.htm

(source:internet, reference only)

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