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首页> 外文期刊>Applied Microbiology >Protective Effects of Lactobacillus plantarum CCFM8610 against Chronic Cadmium Toxicity in Mice Indicate Routes of Protection besides Intestinal Sequestration
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Protective Effects of Lactobacillus plantarum CCFM8610 against Chronic Cadmium Toxicity in Mice Indicate Routes of Protection besides Intestinal Sequestration

机译:植物乳杆菌CCFM8610对小鼠慢性镉毒性的保护作用表明了除肠道隔离外的保护途径

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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.
机译:我们之前的研究证实了植物乳杆菌CCFM8610可以防止小鼠遭受急性镉(Cd)毒性。本研究旨在评估CCFM8610对小鼠慢性Cd毒性的保护作用,并深入了解该菌株的保护方式。将实验小鼠分为两组,并通过饮用水或腹膜内注射将其暴露于Cd中8周。两组都进一步分为四个亚组:对照组,仅Cd,仅CCFM8610和Cd加CCFM8610。测量了粪便,肝脏和肾脏中的镉水平,并注意到了几种镉毒性生物标志物的变化。结果表明,口服Cd时,与Cd和CCFM8610共同处理可有效降低肠道Cd吸收,减少Cd在组织中的积累,减轻组织氧化应激,逆转肝肾损害,并减轻相应的组织病理学变化。当腹膜内引入Cd时,CCFM8610的给药对组织Cd的积聚没有影响,也不会逆转抗氧化酶的活性。然而,CCFM8610仍然提供抗氧化应激的保护,并逆转了Cd毒性生物标志物和组织病理学的改变。这些结果表明,CCFM8610对小鼠的慢性镉毒性有效。除了肠道中的Cd隔离外,CCFM8610处理还提供了针对Cd诱导的氧化应激的直接保护。我们还提供证据表明,后者不太可能通过针对Cd诱导的抗氧化酶活性变化的保护来介导。

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