| 3-Chloro-1,2-propanediol(3-MCPD)is a food processing hazard and is considered a major source of food contamination and a potential carcinogen and/or genotoxic substance.It is present in refined fats and oils and in foods containing these fats and oils,as well as in wet-strength resin-treated paper and cardboard food packaging materials,while previous in vivo toxicological experiments have shown that 3-MCPD and its esters are harmful to the kidneys,nerves,liver and even testes of male animals to varying degrees,but studies on its toxicity mechanisms are shallow and inconclusive.Also because of these toxic effects,it has caused concern for people’s own health.Caenorhabditis elegans,as a highly sensitive and representative model organism in the scientific community,has been widely used in the toxicological assessment and mechanism studies of various hazards.In this study,the toxic mechanism of 3-MCPD was initially investigated by the growth and developmental status,locomotor behavior performance,reproductive ability and endogenous antioxidant level of the nematode,and further investigated the mechanism of toxicity in terms of molecular regulation and metabolism through transcriptome with the help of RNA sequencing technology.The main results are as follows.1.By short-term exposure to wild-type Cryptobacterium hidradenum at different concentrations of 3-MCPD,we found that 200 m M 3-MCPD significantly shortened the mean lifespan of wild-type Cryptobacterium hidradenum,while the effects on body length and body width,number of eggs carried in the uterus,crawling and population number of nematodes were concentration-dependent,with higher concentrations causing some irreversible physiological toxicity to the nematodes.2.After treating Cryptobacterium hidradi with the same exposure,we further investigated biochemical indices including oxidative stress and oxidative damage,and the results showed that ROS levels and lipid peroxidation levels in nematodes increased to different degrees with increasing 3-MCPD concentrations,while the activities of SOD,GSH-PX,and CAT antioxidant enzymes decreased significantly in the exposed group.3.We explored the effect of different concentrations of 3-MCPD on the lifespan of gene deletion mutant nematodes,the expression of lifespan-related genes under200 m M 3-MCPD exposure,the nuclear entry of DAF-16 and HSP-16.2 proteins,and RNA-seq technology.The toxicity mechanism of MCPD,the results showed that3-MCPD did not reduce the lifespan of daf-2 deletion mutants and daf-16 deletion mutants,but significantly inhibited the nuclear entry of the core transcription factor DAF-16,and its downstream HSP-16.Metastasis had no effect,but significantly reduced the expression of genes related to regulating lifespan,a finding that proves that the life-affecting mechanism may be through the insulin pathway,as can be seen from the results of GO enrichment of 3-MCPD exposure through BP,CC and MF The pathway mainly affects the energy metabolism process.These processes involve the synthesis and consumption of biological macromolecules,leading to the growth and developmental damage of C.elegans.From the KEGG enrichment,we found that the most significant pathway is cytochrome P450,which may be the nematode Activates its own detoxification process.In summary,our results suggest that 3-MCPD may cause some toxic damage to C.elegans due to oxidative stress,while the inhibition of insulin signaling pathways,disruption of energy metabolism,and activation of the body’s own detoxification process may be the main causes of rapid aging and death in C.elegans.Our results may also provide a new research model for the toxicity study of other food processing contaminants and provide more favorable evidence for more accurate control of the toxicity mechanism of food processing contaminants. |
