Obesogenic effects of chlorpyrifos and its metabolites during the differentiation of 3T3-L1 preadipocytes.

Chlorpyrifos (CPF) is an organophosphorus pesticide widely and extensively used in agriculture in more than one hundred countries and found ubiquitously in the environment. The present study was aimed at providing a better understanding of the obesogenic potential of CPF and its metabolites, as well as to evaluate their effects on the adipocyte differentiation process. For it, during the initial differentiation process, 3T3-L1 mouse preadipocytes were exposed to different concentrations of CPF, CPF-oxon (CPO), or 3,5,6-trichloropyridinol (TCP), which did not affect cell survival.

Oral exposure to silver nanoparticles increases oxidative stress markers in the liver of male rats and deregulates the insulin signalling pathway and p53 and cleaved caspase 3 protein expression.

The present study was aimed at assessing the impact of AgNPs on the liver of male rats orally exposed to 0, 50, 100 and 200 mg/kg/day of polyvinyl pyrrolidone coated AgNPs (PVP-AgNPs) for 90 days. The induction of apoptotic cell death -by measuring the protein levels of the active form of caspase 3- and the levels of the microtubule-associated protein 1A/1B-light chain (LC3) protein were measured as a marker of the induction of autophagy. PVP-AgNPs caused an increase of the activity of superoxide dismutase (SOD) and catalase (CAT) in the liver of male rats.

New mechanistic insights on the metabolic-disruptor role of chlorpyrifos in apoE mice: a focus on insulin- and leptin-signalling pathways.

Recently, we have provided evidence, suggesting that mice expressing the human apolipoprotein E3 (apoE3) are more prone to develop an obesity-like phenotype and a diabetic profile when subchronically fed a chlorpyrifos (CPF)-supplemented diet. The aim of the current study was to examine the underlying mechanisms through which CPF alters both insulin- and leptin-signalling pathways in an APOE-dependent manner. Both adult apoE3- and E4-targeted replacement and C57BL/6 mice were exposed to CPF at 0 or 2 mg/kg body weight/day through the diet for 8 consecutive weeks.

PRE-CLINICAL SKILLS: A competency-based assessment integrated course implemented early in the curriculum to prepare second-year medical students prior to entering clinical settings.

This article was migrated. The article was marked as recommended. This describes the experience of University School of Medicine (URV) with the early introduction of pre-clinical skills learning in the undergraduate medical curricula to monitor and assessing these competencies as a prerequisite for medical students accessing their training in clinical settings.

Polyvinyl pyrrolidone-coated silver nanoparticles in a human lung cancer cells: time- and dose-dependent influence over p53 and caspase-3 protein expression and epigenetic effects.

The present study was aimed at providing a better understanding of the influence of silver nanoparticles (AgNPs) on the p53 tumor suppressor protein. Cell line A549 was exposed to a range of concentrations of AgNPs, and a time course (up to 72 h) of cell viability was determined. We also determined the time course of gene and protein expression of p53, p21, murine double minute 2 (MDM2) and caspase-3.

Oral subchronic exposure to silver nanoparticles in rats.

Because of their extremely small size, silver nanoparticles (AgNPs) show unique physical and chemical properties, with specific biological effects, which make them particularly attractive for being used in a number of consumer applications. However, these properties also influence the potential toxicity of AgNPs. In this study, we assessed the potential toxic effects of an in vivo oral sub-chronic exposure to polyvinyl pyrrolidone coated AgNPs (PVP-AgNPs) in adult male rats.

Oxidative stress markers after a race in professional cyclists.

The aim was to determine the levels and activities of the oxidative stress markers in erythrocytes, plasma, and urine after a flat cyclist stage. Eight voluntary male professional trained-cyclists participated in the study. Exercise significantly increased erythrocyte, leukocyte, platelet, and reticulocyte counts.

Perinatal exposure to BDE-99 causes decreased protein levels of cyclin D1 via GSK3β activation and increased ROS production in rat pup livers.

We here examined the potential liver toxicity in rat pups from dams exposed during the gestational and lactation periods to 2,2',4,4',5-pentabromodiphenyl ether (BDE-99). Dams were exposed to 0, 1, and 2mg/kg/day of BDE-99 from gestation day 6 to postnatal day 21. When the pups were weaning, the liver from 1 pup of each litter was excised to evaluate oxidative stress markers and the messenger RNA (mRNA) expression of multiple cytochrome P450 (CYP) isoforms.

Perinatal exposure to BDE-99 causes learning disorders and decreases serum thyroid hormone levels and BDNF gene expression in hippocampus in rat offspring.

Exposure of pregnant women to polybrominated diphenyl ethers (PBDEs) may mean serious health risks. The main goal of the present study was to examine the neurobehavioral changes in rat offspring that were perinatally exposed to one of the most prevalent PBDEs congeners found in humans, 2,2',4,4',5-pentaBDE (BDE-99). Rat dams were exposed to 0, 1 and 2mg/kg/day of BDE-99 from gestation day 6 to post-natal day 21.

Gestational exposure to BDE-99 produces toxicity through upregulation of CYP isoforms and ROS production in the fetal rat liver.

On gestation day (GD) 6 to GD 19, pregnant Sprague Dawley rats were orally exposed to 0, 0.5, 1, and 2 mg/kg/day to one of the most prevalent polybrominated diphenyl ethers congeners found in humans, 2,2',4,4',5-pentaBDE (BDE-99). All dams were euthanized on GD 20, and live fetuses were evaluated for sex, body weight, and external, internal, and skeletal malformations and developmental variations.

BDE-99 deregulates BDNF, Bcl-2 and the mRNA expression of thyroid receptor isoforms in rat cerebellar granular neurons.

Although the disruption of thyroid hormone (TH) signaling can largely explain the neurotoxic effects of polybrominated diphenyl ethers (PBDEs), there are still many unknowns about how this interference occurs. In this study, we expose a primary culture of rat cerebellar granule neurons (CGNs) to a 25μM concentration of one of the most prevalent PBDE congeners in humans, 2,2',4,4',5-pentaBDE (BDE-99). The main goal was to investigate the time course of BDE-99 toxicity in relation to the disruption of thyroid receptor (TR) function over 24h.

Effects of BDE-99 on hormone homeostasis and biochemical parameters in adult male rats.

In this study, we evaluated the effects of BDE-99 on hormone homeostasis, as well as in urinary and serum biochemical parameters of adult male rats. Animals (10 per group) received BDE-99 by gavage at single doses of 0, 0.6 and 1.

Effects of exposure to BDE-99 on oxidative status of liver and kidney in adult rats.

Little is known about the potential toxicity of polybrominated diphenyl ethers (PBDEs) on hepatic and renal tissues. In this study, we investigated the modifications in endogenous antioxidant capacity and oxidative damage in liver and kidney of rats by exposure to one of the most persistent PBDE congeners, the 2,2',4,4',5-pentabromodiphenyl ether (BDE-99). Adult male rats (10 per group) received BDE-99 by gavage at a single dose of 0, 0.

Behavioral effects and oxidative status in brain regions of adult rats exposed to BDE-99.

Polybrominated diphenyl ethers (PBDEs) are used as flame retardants. Although developmental neurotoxicity of PBDEs has been already investigated, little is still known about their potential neurotoxic effects in adulthood. In this study, we assessed the oxidative damage in brain sections and the possible behavioral effects induced by exposure to 2,2',4,4',5-pentabromodiphenyl ether (BDE-99).

Lipid peroxidation and antioxidant status in kidney and liver of rats treated with sulfasalazine.

Sulfasalazine (SASP) is a drug commonly used in the treatment of inflammatory bowel diseases (IBD). In this study, the changes in endogenous antioxidant capacity and oxidative damage in liver and kidney of SASP-treated rats were investigated. Adult male Sprague-Dawley rats were orally given 0, 300, or 600 mg SASP/kg body weight for 14 days.

Sulfasalazine induced oxidative stress: a possible mechanism of male infertility.

The mechanism of action of sulfasalazine (SASP) in male infertility is not well elucidated. For it, an oxidative stress-like mechanism inductor of infertility was hypothesized. Adult male Sprague-Dawley rats (20/group) were orally administered 0, 300, and 600mg SASP/kg body weight for 14 days.

Melatonin reduces uranium-induced nephrotoxicity in rats.

The protective role of exogenous melatonin on U-induced nephrotoxicity was investigated in rats. Animals were given single doses of uranyl acetate dihydrate (UAD) at 5 mg/kg (subcutaneous), melatonin at 10 or 20 mg/kg (intraperitoneal), and UAD (5 mg/kg) plus melatonin (10 or 20 mg/kg), or vehicle (control group). In comparison with the UAD-treated group only, significant beneficial changes were noted in some urinary and serum parameters of rats concurrently exposed to UAD and melatonin.

Pro-oxidant effects in the brain of rats concurrently exposed to uranium and stress.

Metal toxicity may be associated with increased rates of reactive oxygen species (ROS) generation within the central nervous system (CNS). Although the kidney is the main target organ for uranium (U) toxicity, this metal can also accumulate in brain. In this study, we investigated the modifications on endogenous antioxidant capacity and oxidative damage in several areas of the brain of U-exposed rats.

Exposure of pregnant rats to uranium and restraint stress: effects on postnatal development and behavior of the offspring.

The effects on postnatal development and behavior were assessed in the offspring of female rats concurrently exposed to uranium (U) and restraint stress. Adult female rats were administered uranyl acetate dihydrate (UAD) in the drinking water at doses of 0, 40 and 80 mg/(kg day) for 4 weeks before mating with untreated males, as well as during pregnancy and lactation. One-half of female rats in each group were concurrently subjected to restraint (2h/day).

Assessment of the pro-oxidant activity of uranium in kidney and testis of rats.

The pro-oxidant activity of uranium (U) was assessed in kidney and testes of male rats, tissues in which toxic effects of this metal are well established. Eight groups of Sprague-Dawley rats received uranyl acetate dihydrate (UAD) in the drinking water at 0, 10, 20, and 40 mg/kgday for 3 months. Rats in four groups were concurrently subjected to restraint during 2 h/day throughout the study.

Restraint stress does not enhance the uranium-induced developmental and behavioral effects in the offspring of uranium-exposed male rats.

The influence of stress on postnatal development and behavior was assessed in the offspring of male rats exposed to uranium (U). Eight groups of adult animals received uranyl acetate dihydrate (UAD) in the drinking water at doses of 0, 10, 20 and 40 mg/kg/day during 3 months. One half of rats in each group were concurrently subjected to restraint stress during 2 h per day throughout the study.

Combined action of uranium and stress in the rat. I. Behavioral effects.

The influence of restraint stress on uranium (U)-induced behavioral effects was assessed in adult male rats. Eight groups of animals received uranyl acetate dihydrate (UAD) in the drinking water at doses of 0, 10, 20 and 40 mg/kg/day during 3 months. Rats in four groups were concurrently subjected to restraint during 2 h per day throughout the study.

Combined action of uranium and stress in the rat. II. Effects on male reproduction.

The effects of stress on the potential reproductive toxicity of long-term exposure to uranyl acetate dihydrate (UAD) were assessed in adult male rats. Six groups of animals were given UAD at 10, 20, and 40 mg/kg/day in the drinking water during 3 months. Animals in three of these groups were also subjected to restraint for 2 h/day during the same period.

Influence of maternal stress on uranium-induced developmental toxicity in rats.

It has been demonstrated that uranium is an embryo/fetal toxicant when given orally or subcutaneously to pregnant mice. On the other hand, maternal stress has been shown to enhance the developmental toxicity of a number of metals. In this study, maternal toxicity and developmental effects of a concurrent exposure to uranyl acetate dihydrate (UAD) and restraint stress were evaluated in rats.

Influence of age on aluminum-induced neurobehavioral effects and morphological changes in rat brain.

Aluminum (Al) is potentially toxic for mammals. In contrast to well documented Al neurotoxicity, neurobehavioral studies of Al in rodents have generally not produced robust or consistent results. In the present study, 16 young male (21 days old) and 16 old male (18 months) rats were exposed to 0 (control group) and 100 mg/kg/day of Al administered as Al nitrate nonahydrate in drinking water concurrently with citric acid (356 mg/kg/day) for a period of 100 days.