Pyrethroids are the third most applied group of insecticides worldwide and are extensively used in agricultural and non-agricultural applications. Pyrethroids exhibit low toxicity to mammals, but have extremely high toxicity to fish and non-target invertebrates. Their high hydrophobicity, along with pseudo-persistence due to continuous input, indicates that pyrethroids will accumulate in sediment, pose long-term exposure concerns to benthic invertebrates and ultimately cause significant risk to benthic communities and aquatic ecosystems. The current review synthesizes the reported sediment concentrations of pyrethroids and associated toxicity to benthic invertebrates on a global scale. Geographically, the most studied area was North America, followed by Asia, Europe, Australia and Africa. Pyrethroids were frequently detected in both agricultural and urban sediments, and bifenthrin and cypermethrin were identified as the main contributors to toxicity in benthic invertebrates. Simulated hazard quotients (HQ) for sediment-associated pyrethroids to benthic organisms ranged from 10.5±31.1 (bifenthrin) to 41.7±204 (cypermethrin), suggesting significant risk. The current study has provided evidence that pyrethroids are not only commonly detected in the aquatic environment, but also can cause toxic effects to benthic invertebrates, and calls for better development of accurate sediment quality criteria and effective ecological risk assessment methods for this emerging class of insecticides.

Lactobacillus acidophilus alleviates type 2 diabetes induced by a high fat diet and streptozotocin (STZ) injection by regulating gut microbiota, hepatic glucose and lipid metabolism in mice.

The global prevalence of obesity is rising year by year, which has become a public health problem worldwide. In recent years, animal studies and clinical studies have shown that some lactic acid bacteria possess an anti-obesity effect. In our previous study, mixed lactobacilli (Lactobacillus plantarum KLDS1.0344 and Lactobacillus plantarum KLDS1.0386) exhibited anti-obesity effects in vivo by significantly reducing body weight gain, Lee's index and body fat rate; however, its underlying mechanisms of action remain unclear. Therefore, the present study aims to explore the possible mechanisms for the inhibitory effect of mixed lactobacilli on obesity. C57BL/6J mice were randomly divided into three groups including control group (Control), high fat diet group (HFD) and mixed lactobacilli group (MX), and fed daily for eight consecutive weeks. The results showed that mixed lactobacilli supplementation significantly improved blood lipid levels and liver function, and alleviated liver oxidative stress. Moreover, the mixed lactobacilli supplementation significantly inhibited lipid accumulation in the liver and regulated lipid metabolism in epididymal fat pads. Notably, the mixed lactobacilli treatment modulated the gut microbiota, resulting in a significant increase in acetic acid and butyric acid. Additionally, Spearman's correlation analysis found that several specific genera were significantly correlated with obesity-related indicators. These results indicated that the mixed lactobacilli supplementation could manipulate the gut microbiota and its metabolites (acetic acid and butyric acid), resulting in reduced liver lipid accumulation and improved lipid metabolism of adipose tissue, which inhibited obesity.

Health and wellbeing are significantly impaired by alcoholic liver disease (ALD), and although some lactic acid bacteria strains have been shown previously to relieve ALD symptoms, the mechanisms behind these effects are still unclear. Here, the Lieber–DeCarli liquid diet containing alcohol was fed to C57BL/6J mice for 6 weeks to build a chronic alcoholic liver lesion model to study the protective effects and possible mechanisms of Lactobacillus mixture (Lactobacillus plantarum KLDS1.0344 and Lactobacillus acidophilus KLDS1.0901). The results showed that Lactobacillus mixture improved intestinal epithelial permeability and reduced the serum lipopolysaccharide (LPS) levels. Furthermore, Lactobacillus mixture inhibited liver lipid accumulation, oxidative stress, and inflammation by regulating AMPK, Nrf-2, and TLR4/NF-κB pathways. Importantly, the Lactobacillus mixture modulated the gut microbiota, resulting in increased short-chain fatty acid (SCFA) producers and decreased Gram-negative bacteria. Taken together, these findings indicated that the Lactobacillus mixture could positively regulate the gut microbiota, causing increased levels of SCFAs, which inhibited alcohol-induced liver lipid accumulation and oxidative stress through the gut–liver axis. Moreover, following administration of the Lactobacillus mixture, the improvement of intestinal epithelial permeability and the reduction of Gram-negative bacteria led to the decrease of LPS entering the portal vein, thereby inhibiting alcohol-induced liver inflammation.