4.6 Article

Protective Effects of Lactobacillus plantarum CCFM8610 against Chronic Cadmium Toxicity in Mice Indicate Routes of Protection besides Intestinal Sequestration

Journal

APPLIED AND ENVIRONMENTAL MICROBIOLOGY
Volume 80, Issue 13, Pages 4063-4071

Publisher

AMER SOC MICROBIOLOGY
DOI: 10.1128/AEM.00762-14

Keywords

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Funding

  1. National Science Fund [31125021]
  2. National Natural Science Foundation of China [31371721]
  3. Science and Nature Foundation in Jiangsu Province [BK 20131102]
  4. key projects in the National Science & Technology Pillar Program during the twelfth 5-year plan period [2013BAD18B01, 2013BAD18B02, 2012BAD28B07]
  5. 111 Project [B07029]
  6. Priority Academic Program Development of Jiangsu Higher Education Institutions
  7. BBSRC [BBS/E/F/00044453] Funding Source: UKRI
  8. Biotechnology and Biological Sciences Research Council [BBS/E/F/00044453] Funding Source: researchfish

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Our previous study confirmed the ability of Lactobacillus plantarum CCFM8610 to protect against acute cadmium (Cd) toxicity in mice. This study was designed to evaluate the protective effects of CCFM8610 against chronic Cd toxicity in mice and to gain insights into the protection mode of this strain. Experimental mice were divided into two groups and exposed to Cd for 8 weeks via drinking water or intraperitoneal injection. Both groups were further divided into four subgroups, control, Cd only, CCFM8610 only, and Cd plus CCFM8610. Levels of Cd were measured in the feces, liver, and kidneys, and alterations of several biomarkers of Cd toxicity were noted. The results showed that when Cd was introduced orally, cotreatment with Cd and CCFM8610 effectively decreased intestinal Cd absorption, reduced Cd accumulation in tissue, alleviated tissue oxidative stress, reversed hepatic and renal damage, and ameliorated the corresponding histopathological changes. When Cd was introduced intraperitoneally, administration of CCFM8610 did not have an impact on tissue Cd accumulation or reverse the activities of antioxidant enzymes. However, CCFM8610 still offered protection against oxidative stress and reversed the alterations of Cd toxicity biomarkers and tissue histopathology. These results suggest that CCFM8610 is effective against chronic cadmium toxicity in mice. Besides intestinal Cd sequestration, CCFM8610 treatment offers direct protection against Cd-induced oxidative stress. We also provide evidence that the latter is unlikely to be mediated via protection against Cd-induced alteration of antioxidant enzyme activities.

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