Liu et al. 2020 - Lactobacillus plantarum CCFM8610 and cadmium excretion

Liu and colleagues tested whether Lactobacillus plantarum CCFM8610 could relieve cadmium-induced intestinal motility dysfunction and reduce cadmium burden in mice. This is probiotic mitigation evidence: it supports a plausible fecal-excretion mechanism for lowering cadmium absorption, but it does not measure metals in probiotic supplements or consumer foods.

Key numbers

Exposure and intervention design

The animal experiment used 30 C57BL/6 mice after a 1-week adaptation period. Mice were divided into three groups: control, Cd, and CCFM8610 plus Cd. Treatments lasted 10 weeks.

The companion cell experiment exposed HT-29 intestinal cells to 50 mM CdCl2 for 24 hours for iTRAQ proteomic analysis. The authors report 168 differentially expressed proteins after Cd exposure using fold-change >2.0 and p < 0.05 screening criteria. Eight heat-shock proteins were upregulated by a factor of 2-3 after Cd exposure, and one apoptosis-related protein was reported as increased by a factor of 8.8.

Intestinal motility and cadmium burden

Chronic oral Cd exposure significantly decreased fecal water content, inhibited small-intestinal transit, and delayed first black stool defecation time in mice. L. plantarum CCFM8610 treatment significantly relieved those Cd-induced intestinal motility changes as shown in Figure 3.

Compared with controls, Cd exposure significantly increased Cd levels in liver, kidney, and blood (p < 0.05). L. plantarum CCFM8610 treatment led to a marked reduction in Cd levels in blood, liver, and kidneys in Figure 6. The PDF text states the statistical direction and significance but does not provide the figure’s bar values as extractable table numbers.

Neurotransmitter and stress-response markers

Cd exposure significantly reduced colonic acetylcholinesterase, vasoactive intestinal peptide, 5-hydroxytryptamine, and substance P, while increasing calcitonin gene-related peptide and nitric oxide. L. plantarum CCFM8610 recovered the levels of those neurotransmitter markers and suppressed cellular stress-response pathways, including MAPK pathway signals.

Methods (brief)

Cd in liver, kidney, and blood was measured by graphite furnace atomic absorption spectrophotometry. Fecal samples were collected weekly to determine fecal water content. Data were reported as means +/- SD and analyzed by one-way ANOVA, with p < 0.05 treated as significant. The animal protocol was approved by the Ethics Committee of Jiangnan University under JN. No. 20170618-20170918.

Implications

Certification: Do not use this source in product occurrence pools for probiotic supplements, foods, or ingredients. The numeric Cd values come from controlled CdCl2 exposure, biological tissues, and intervention outcomes, not market product sampling.

App: Useful context for mitigation explainers where specific probiotic strains may increase fecal cadmium excretion or reduce tissue cadmium burden after dietary exposure.

Courses: Useful teaching example for separating mechanistic animal evidence from occurrence evidence and for avoiding extraction of unreported figure bar values.

Wiki pages this source may touch

• formulation
• remediation-evidence
• cadmium
• index

Verification notes

This page was built from the full PDF text, including the abstract, animal experiment protocol, Table 2, Figure 3 and Figure 6 captions/results text, Cd measurement methods, and discussion. Products and ingredients are intentionally empty because the study tests CdCl2 exposure and probiotic intervention in mice and cells. The source reports figure-only Cd burden outcomes; the page records direction and significance without estimating bar heights from the figure image.

Page history

The five most recent substantive edits to this page. The full version history lives in git; when DOI minting comes online (see schema docs), each entry below will also link to a version-pinned DataCite DOI.