ABSTRACT
Cadmium (Cd), is a highly toxic environmental pollutant, which seriously threatens the health of poultry and humans. The occurrence of osteoporosis is the main manifestation of cadmium toxicity. Pyroptosis plays an important role in the development of osteoporosis. Melatonin has been shown to affect preserving bone health. However, the underlying mechanism has not been elucidated. In the present study, these functions of melatonin have been investigated in duck bone tissue and osteoblast during cadmium exposure. In vivo, the studies suggest that melatonin protects against cadmium-induced duck osteoporosis by improving the osteogenesis function, inhibiting bone resorption, and suppressing the occurrence of pyroptosis. In vitro, the findings demonstrated that melatonin alleviated the inhibition effect of cadmium on duck bone marrow-derived mesenchymal stem cells (BMSC) osteogenic differentiation, and suppressed the cadmium-induced osteoclast differentiation. In addition, we also found that melatonin prevents cytokines release of lactate dehydrogenase (LDH), interleukin-18 (IL-18), and interleukin-1ß (IL-1ß) by cadmium-induced, and reduces the expression of n-terminal Gasdermin D (N-GSDMD), alleviates the osteoblast death rate. In short, melatonin as a potential therapeutic agent has bright prospects in cadmium-induced bone toxicity.
ABSTRACT
Salmonella typhimurium, as a major foodborne pathogen, poses a serious threat to public health safety worldwide. Here, we present a colorimetric biosensor based on aptamer recognition-induced multi-DNA release and peroxidase-mimicking three-way junction DNA-silver/platinum bimetallic nanoclusters (3WJ/DNA-Ag/PtNCs) for the detection of S. typhimurium. In this method, S. typhimurium specifically binds to the aptamer and releases multiple cDNAs to form the three-way junction DNA structure and synthesize silver/platinum bimetallic nanoclusters, which induces signaling changes. Interestingly and importantly, the use of 3WJ/DNA as the template for synthesizing Ag/PtNCs gives the method an extremely low background signal. Under the optimal conditions, the constructed biosensor had a linear response range of 2.6 × 102-2.6 × 106 CFU/mL and a detection limit of 2.6 × 102 CFU/mL for the detection of S. typhimurium. In addition, the proposed method can effectively detect S. typhimurium in milk.
Subject(s)
Aptamers, Nucleotide , Biosensing Techniques , Colorimetry , Metal Nanoparticles , Platinum , Salmonella typhimurium , Silver , Salmonella typhimurium/isolation & purification , Biosensing Techniques/methods , Aptamers, Nucleotide/chemistry , Colorimetry/methods , Platinum/chemistry , Silver/chemistry , Metal Nanoparticles/chemistry , Milk/microbiology , Milk/chemistry , Limit of Detection , DNA/chemistry , Animals , Peroxidase/chemistry , Peroxidase/metabolismABSTRACT
Matrix-assisted laser desorption ionization time-of-flight mass spectrometry has been widely used as an emerging technology for the rapid identification of microorganisms. Cronobacter sakazakii (C. sakazakii) is a food-borne pathogen of particular importance to the powdered infant formula (PIF) processing environment due to its high lethality in infants. However, the traditional solid spotting detection method of pretreating samples for MALDI-TOF MS leads only to qualitative detection of C. sakazakii. We developed a new, low-cost, robust liquid spotting pretreatment method and used a response surface methodology to optimize its parameters. The applicability, accuracy, and quantitative potential were measured for different types of samples. The optimal parameters of this method were as follows: a volume of 70% formic acid of 25 µL, treatment with ultrasound at 350 W for 3 min, and a volume of acetonitrile added of 75 µL. These conditions led to the highest identification score for C. sakazakii (1926.42 ± 48.497). This method was found to detect bacteria accurately and reproducibly. When 70 strains of C. sakazakii isolates were analyzed with this method, the identification accuracy was 100%. The detection limit of C. sakazakii in environmental and PIF samples was 4.1 × 101 cfu/mL and 2.72 × 103 cfu/mL, respectively.
ABSTRACT
Environmental and occupational exposure to cadmium has been shown to induce kidney damage, liver injury, neurodegenerative disease, and osteoporosis. However, the mechanism by which cadmium induces autophagy in these diseases remains unclear. Studies have shown that cadmium is an effective inducer of oxidative stress, DNA damage, ER stress, and autophagy, which are thought to be adaptive stress responses that allow cells exposed to cadmium to survive in an adverse environment. However, excessive stress will cause tissue damage by inducing apoptosis, pyroptosis, and ferroptosis. Evidently, oxidative stress-induced autophagy plays different roles in low- or high-dose cadmium exposure-induced cell damage, either causing apoptosis, pyroptosis, and ferroptosis or inducing cell survival. Meanwhile, different cell types have different sensitivities to cadmium, which ultimately determines the fate of the cell. In this review, we provided a detailed survey of the current literature on autophagy in cadmium-induced tissue damage. A better understanding of the complex regulation of cell death by autophagy might contribute to the development of novel preventive and therapeutic strategies to treat acute and chronic cadmium toxicity.
