Food and Chemical Toxicology最新文献

Lifelong, the general population is exposed to mixtures of chemicals. Most often, risk assessment is performed to estimate the probability of adverse effects in the population using external exposures to a single chemical and considering one route of exposure. To estimate whole exposure to a chemical, human biomonitoring studies are used to measure chemical concentrations in biological matrices. The limitations of these studies are that is not possible to distinguish the sources or the routes of exposure. Moreover, only the concentrations of a limited number of chemicals are usually determined due to the associated cost. In this study, a methodology has been developed to estimate the internal exposures of the population to a mixture of trace elements (inorganic As, Cd, Pb and Hg) throughout lifetime. This methodology uses realistic lifetime exposure trajectories coupled to physiological based kinetic modeling, considering several sources of exposure. Then, the estimated biomarkers of exposure were compared to human biomonitoring data to estimate the robustness of the methodology. Finally, risk characterization was performed based on the simulated biomarkers of exposure considering an additive effect of chemicals. This methodology allows to determine the contribution of chemicals to the overall risk of renal effect.

Gardenia blue (GB), a widely used plant-derived food color is prepared by reaction of genipin, the aglycone of geniposide, with protein hydrolysate. Recent animal studies investigating GB toxicity have indicated blue coloration in the gastrointestinal tract, kidneys and mesenteric lymph nodes in rodents following dietary administration. This study investigated the uptake and disposition of [¹⁴C]GB in male and female rats and mice administered 100 or 1000 mg/kg by gavage. [¹⁴C]GB was prepared by reaction of [2-¹⁴C]genipin with soy protein hydrolysate. Following administration in rats, ¹⁴C was eliminated primarily in feces (89-97% of administered dose), exhaled volatile organic chemical (VOC) and CO₂ traps contained no radioactivity, and urine contained 0.2-0.4 %. In bile-duct-cannulated rats (100 mg/kg [¹⁴C]GB), 0.25% of dose was recovered in bile, and in urine, 0.5%. The percent of the dose absorbed was 0.9%, based on radioactivity in urine, bile, and carcass minus digestive tract contents. The highest level of radioactivity in tissues was in kidney; however renal recovery was low, with only 0.02-0.04% of the dose recovered in kidney. Repeated dosing indicated that ¹⁴C accumulated in kidney, and was slowly removed following cessation of dosing, consistent with previous studies, in the absence of any functional or histopathological changes.

Rutin (Rut) is a flavonoid with pharmacological activities such as anti-inflammatory and antioxidant. Acrylamide (ACR) is a toxic substance widely found in human life that can induce neurotoxicity. Some studies have confirmed that neurotoxicity caused by ACR induces myelin damage, which in turn causes neurological dysfunction. Therefore, we established a rutin intervention model to investigate the protective effect of Rut on ACR-induced sciatic nerve injury in rats and its mechanism. The results showed that superoxide dismutase (SOD) activity and glutathione (GSH) content increased and lactate dehydrogenase (LDH) activity decreased in the middle and high dose groups of Rut compared with the ACR group, and the expression of Myelin basic protein (MBP), Extracellular-regulated kinase 1/2(ERK1/2), Phosphorylated extracellular regulated kinase 1/2 (P-ERK1/2), and Nuclear factor E-2-associated factor (Nrf2) was promoted in the Rut-protected group, which suggests that Rutin has a protective effect on ACR-induced sciatic nerve injury and that the mechanism of Rutin's protective effect is related to activation of the ERK1/2 pathway and alleviation of oxidative stress injury.