elegans is similar to that observed in mammals, , implying that the toxicological studies performed in C.
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A series of studies have found that toxicity for toxicants in C. elegans is useful for toxicological studies from whole-animal level down to single cell level. A number of toxicity studies have been conducted with the aid of both lethal and sub-lethal endpoints for metallic salts –, organic compounds –, drugs –, and engineered nanomaterials –. elegans has been widely accepted and utilized as an important alternative animal model for toxicity testing, –. elegans as a model animal has attracted the increased attention in the fields of both biomedical science and toxicology –. Nematode Caenorhabditis elegans, an important model animal used in various fields, has invariant and fully described developmental program, well-characterized genome, short and prolific life cycle, and small body size –. However, so far no toxicological study on ractopamine has been performed. Overexpression of calpastatin in skeletal muscle of mice prevented clenbuterol-induced muscle hypertrophy and phenotypic shift. The preferential involvement of calpain 2 autolysis was found for clenbuterol-induced skeletal muscle remodelling in rats. Clenbuterol not only enhanced muscle fiber size but also increased expression of GATA-2 protein in skeletal muscle of rat uterus. Clenbuterol caused an impairment of collagen turnover by down-regulating MMP-9 activity. Dietary administration of clenbuterol decreased androgen receptor (AnR) expression in testicle, glucocorticoid receptor (GR) expression in lymphoid tissues, and β-adrenergic receptor (β-AR) expression in targeted organs of chickens. Administration of growth-promoting doses of clenbuterol adversely affected the liver function in female pigs. Several toxicological studies have been performed for clenbuterol. More recently, it was further reported that ractopamine administration might cause the myocardial toxicity in dogs.
Moreover, at least the toxic effects on cardiovascular systems (such as tachycardia and hypertension) are considered to be of clinical relevance –. Following consumption of meat or liver from clenbuterol administrated cattle, intoxication cases were described. The in vitro study has indicated that clenbuterol exhibited potential toxicity on structure and function of trypsin, an important digestive enzyme, and stimulated guinea-pig heart rate. Īmong the used weight loss agents, clenbuterol and ractopamine belong to products that may have health hazards upon accidental or intentional exposure and ingestion. Ractopamine, a synthetic β2-adrenoceptor agonist, is now widely used as a feed additive in the United States to promote a reduction in body fat and to enhance muscle growth in cattle, pigs, or turkeys. With the increased use of internet sales, the internet has made this even banned product to be readily accessible for the aim of weight loss or dieting addition. Clenbuterol, a typical weight loss agent, is a kind of β2-adrenergic agonist, and was illegally used as a feed additive to improve production performance and a carcass composition in many countries –. Illegal or unsuitable use of weigh loss agents has gradually become a public health concern –. elegans assay system may be useful for assessing the possible toxicity from weight loss agents, and clentuberol and ractopamine may induce toxicity through different molecular mechanisms. Ractopamine more severely decreased expression levels of daf-16, sgk-1, skn-1, and aak-2 genes than clentuberol, and increased expression levels of daf-2 and age-1 genes at the examined concentration. Besides oxidative stress, we found that clentuberol might reduce lifespan through influencing insulin/IGF signaling pathway however, ractopamine might reduce lifespan through affecting both insulin/IGF signaling pathway and TOR signaling pathway.
Overexpression of sod-2 gene encoding a Mn-SOD to prevent induction of oxidative stress effectively inhibited toxicity from clentuberol or ractopamine. At relatively high concentrations, ractopamine exhibited more severe toxicity than clentuberol on nematodes. Although acute exposure to the examined concentrations of clentuberol or ractopamine did not induce lethality, prolonged exposure to 10 µg/L of clentuberol and ractopamine reduced lifespan. Both acute and prolonged exposures to clentuberol or ractopamine decreased brood size and locomotion behavior, and induced intestinal autofluorescence and reactive oxygen species (ROS) production. In the present study, we used Caenorhabditis elegans assay system to investigate in vivo toxicity from clentuberol and ractopamine and the possible underlying mechanism.
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