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

Abstract

cOur 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.

Oral Administration of Probiotics Inhibits Absorption of the Heavy Metal Cadmium by Protecting the Intestinal Barrier

“…Our previous study confirmed the ability of a probiotic, L. plantarum CCFM8610, to inhibit Cd absorption in the intestines of mice, and the protective mechanism is partly due to the intestinal sequestration by the Cd-binding ability of the strain (15,16). This study was performed to evaluate whether probiotics can inhibit Cd absorption through other routes besides Cd binding, with a focus on protection of the gut barrier.…”

“…On the other hand, other studies have demonstrated that probiotics can protect against intestinal barrier disruption and decrease intestinal permeability by alleviating oxidative stress in animals (49,50). It has been confirmed that L. plantarum CCFM8610 exhibits good antioxidative ability in vitro and in vivo (14,15). Such an ability may protect it from the chain effects triggered by Cd-induced oxidative stress in the intestines.…”

“…The strains were cultured in de Man, Rogosa, and Sharpe (MRS) broth (Hope Bio-technology Company, Qingdao, China) at 37°C for 18 h. All of the bacteria were subcultured twice before the experiment. For application of the strains in the animal experiments, the cells were cultured and lyophilized with skim milk as a protectant (15).…”

“…Our previous work reported the protective effects of a probiotic against Cd toxicity, demonstrating that Lactobacillus plantarum CCFM8610, a selected probiotic with good Cd-binding and antioxidative capabilities (14), can significantly inhibit Cd absorption in the intestines of mice, which in turn decreases Cd accumulation in tissues and alleviates Cd-induced tissue histopathology (15,16). The Cd-binding ability of CCFM8610 appears to be important for the inhibition of intestinal Cd absorption, because it enables CCFM8610 to sequester Cd before intestinal absorption and increase Cd excretion as Lactobacillus strains are excreted through feces (17).…”

Cadmium-induced apoptosis of Siberian tiger fibroblasts via disrupted intracellular homeostasis

“…Long-term exposure to Cd 2+ causes a variety of pathological conditions and poisons many cell types, including kidney, liver, brain, testis, lung, and thymus, both in vitro and in vivo [4–6]. Cd 2+ compounds promote tumorigenesis in the testes, lungs, and prostate as well as hematopoietic malignancies [7]. They also morphologically transform and induce chromosomal aberrations and gene mutations in cultured mammalian cells [8].…”