Disruption of oogenesis and molting by methoprene and glyphosate in Gammarus fossarum: involvement of retinoic acid?

In the last decade, the freshwater amphipod Gammarus fossarum proved to be a promising sentinel species in active biomonitoring programs to assess the effects of environmental contamination on non-target organisms. Given that the highly conserved retinoid (RETs) metabolism supports many biological functions and is perturbed by xenobiotics and used as biomarker for vertebrates, we explored the RETs functions in the crustacean model Gammarus fossarum. More specifically, we studied the implication of all -trans retinoic acid (atRA) in the reproduction (embryo, oocyte, and juvenile production) and development (success and delay of molting) by exposing G.

The retinoid metabolism of Gammarus fossarum is disrupted by exogenous all-trans retinoic acid, citral, and methoprene but not by the technical formulation of glyphosate.

Over the last decade, fluctuations of retinoids (RETs), also known as vitamin A and derivatives, have proved to be useful biomarkers to assess the environmental chemical pressure on a wide variety of non-target vertebrates. This use of RET-based biomarkers is of particular interest in the non-target sentinel species Gammarus fossarum in which RETs were shown to influence crucial physiological functions. To study and probe this metabolism in this crustacean model, a UHPLC-MS/MS method was developed to 1) identify and 2) monitor several endogenous RETs in unexposed females throughout their reproductive cycle.

Pesticides Inhibit Retinoic Acid Catabolism in PLHC-1 and ZFL Fish Hepatic Cell Lines.

The population of yellow perch () in lake Saint-Pierre (QC, Canada) has been dramatically declining since 1995 without any sign of recovery. Previous studies have shown disrupted retinoid (vitamin A) metabolic pathways in these fish, possibly due to the influence of pesticides. Our study aimed to evaluate the impact of some herbicides and neonicotinoids on retinoic acid catabolism in the fish hepatic cell lines PLHC-1 and ZFL.

Cadmium affects autophagy in the human intestinal cells Caco-2 through ROS-mediated ERK activation.

Cadmium is a toxic metal that enters the food chain. Following oral ingestion, the intestinal epithelium has the capacity to accumulate high levels of this metal. We have previously shown that Cd induces ERK1/2 activation in differentiated but not proliferative human enterocytic-like Caco-2 cells.

Zinc interference with Cd-induced hormetic effect in differentiated Caco-2 cells: Evidence for inhibition downstream ERK activation.

Cadmium (Cd) is a toxic metal that enters the food chain. Following oral ingestion, the intestinal epithelium represents an effective protective barrier against Cd toxicity, but it is also a target tissue that may accumulate and trap high levels of the ingested metal. Using human enterocytic-like Caco-2 cells, we have previously shown that Cd may induce a concentration and time-dependent increase in 3-(4,5-dimethyl-2-thiazol-2-yl)-2,5-diphenyltetrazolium bromide assay (MTT)-reducing activity in differentiated cultures with correlation to ERK1/2 activation.

Foraging in maize field areas: A risky business?

In Quebec, Canada, the cultivation of maize dominates the agricultural territory. This crop requires a sustained supply of fertilizers from different sources: chemical, natural or from residual materials (sludge). These amendments contain metallic trace elements, which may lead to metal-contaminated maize pollen, a possible source of prooxidants for the foraging bees.

Diamine Oxidase from White Pea (Lathyrus sativus) Combined with Catalase Protects the Human Intestinal Caco-2 Cell Line from Histamine Damage.

Diamine oxidase (DAO) administration has been proposed to treat certain gastrointestinal dysfunctions induced by histamine, an immunomodulator, signaling, and pro-inflammatory factor. However, HO resulting from the oxidative deamination of histamine by DAO may be toxic. The purpose of this study was to investigate to which extent DAO from white pea (Lathyrus sativus), alone or in combination with catalase, may modulate histamine toxicity in the human intestinal Caco-2 cell line.

Mixtures of herbicides and metals affect the redox system of honey bees.

The increasing loss of bee colonies in many countries has prompted a surge of studies on the factors affecting bee health. In North America, main crops such as maize and soybean are cultivated with extensive use of pesticides that may affect non-target organisms such as bees. Also, biosolids, used as a soil amendment, represent additional sources of metals in agroecosystems; however, there is no information about how these metals could affect the bees.

Low dietary levels of Al, Pb and Cd may affect the non-enzymatic antioxidant capacity in caged honey bees (Apis mellifera).

Several hypotheses have been proposed to explain the abnormally high mortality rate observed in bee populations in Europe and North America. While studies based on the effects of pesticides are paramount, the metals present in agroecosystems are often overlooked. Sources of metals are linked to the nature of soils and to agricultural practices, namely the use of natural or chemical nutrients as well as residual materials from waste-water treatment sludge.

Effects of realistic doses of atrazine, metolachlor, and glyphosate on lipid peroxidation and diet-derived antioxidants in caged honey bees (Apis mellifera).

The decline in the population of pollinators is a worrying phenomenon worldwide. In North America, the extensive use of herbicides in maize and soya crops may affect the health of nontarget organisms like the honey bee. In this study, caged honey bees were exposed to realistic doses of atrazine, metolachlor, and glyphosate for 10 days via contaminated syrup.

Different mechanisms for metal-induced adaptation to cadmium in the human lung cell lines A549 and H441.

Sensitivity to Cd and Zn as well as the capacity to develop tolerance were characterized in human lung cells A549 and H441. In the A549 cells, a 2-fold lower LC(50) was obtained for Cd compared to Zn, whereas H441 cells were similarly sensitive to both metals. H441 cells were twice as resistant to Cd as the A549 cells.

Expression of macrophage migration inhibitory factor by osteoblastic cells: protection against cadmium toxicity.

Exposition to cadmium (Cd) has been linked to bone metabolism alterations and occurrence of osteoporosis. Despite its known renal toxicity which indirectly disrupts bone metabolism through impairment of vitamin D synthesis, increasing evidence argues for the direct action of Cd on bone-forming osteoblasts. Indeed, accumulation of Cd in osteoblasts and metal-induced cell death has been documented but little is known about the intracellular mechanisms of protection against this stress.

Fe- and Zn-induced inhibition of Cd uptake in human lung cell lines: speciation studies with H441 and A549 cells.

Cadmium transport was studied in human lung cell lines A549 and H441 as a function of inorganic metal speciation. A 2-fold higher equilibrium accumulation was obtained in the A549 cells, but a specific system of transport of high affinity and low capacity was characterized in both these cells. Exposure conditions optimizing [Cd2+] increased Cd uptake, but CdCln2-n species are also taken up.

Characterization of basolateral-to-apical transepithelial transport of cadmium in intestinal TC7 cell monolayers.

Cadmium (Cd) is a toxic metal with an extremely long half-life in humans. The intestinal absorption of Cd has been extensively studied but the role the intestinal epithelium may play in metal excretion has never been considered. The basolateral (BL)-to-apical (AP) transepithelial transport of Cd was characterized in TC7 human intestinal cells.

Involvement of transient receptor potential melastatin-related 7 (TRPM7) channels in cadmium uptake and cytotoxicity in MC3T3-E1 osteoblasts.

Exposure to cadmium (Cd) disrupts bone metabolism, causing osteoporosis. Impaired vitamin D metabolism was initially proposed as the underlying mechanism, yet recent studies argue for the direct effect of Cd on bone cells. This study aimed at characterizing (109)Cd uptake and cytotoxicity in MC3T3-E1 osteoblasts.

Cadmium-induced hormetic effect in differentiated Caco-2 cells: ERK and p38 activation without cell proliferation stimulation.

Cadmium (Cd) is a toxic metal that enters the food chain. Following oral ingestion, the intestinal epithelium may in part protect against Cd toxicity but is also a target tissue. Using human enterocytic-like Caco-2 cells, we have previously shown differences in sensitivity to Cd according to the differentiation status.

Resistance to cadmium as a function of Caco-2 cell differentiation: role of reactive oxygen species in cadmium- but not zinc-induced adaptation mechanisms.

Cadmium (Cd) is a highly toxic metal that enters the food chain. Following oral ingestion, the intestinal epithelium is the first biological barrier crossed by Cd and is also an important target tissue. In the present study, the human intestinal Caco-2 cell line was used to evaluate the impact of a low level of exposure on both undifferentiated and differentiated intestinal cells.

Characterization of cadmium uptake and cytotoxicity in human osteoblast-like MG-63 cells.

Since bone mass is maintained constant by the balance between osteoclastic bone resorption and osteoblastic bone formation, alterations in osteoblast proliferation and differentiation may disturb the equilibrium of bone remodeling. Exposure to cadmium (Cd) has been associated with the alteration of bone metabolism and the development of osteoporosis. Because little information is available about the direct effects of Cd on osteoblastic cells, we have characterized in vitro the cellular accumulation and cytotoxicity of Cd in human osteoblastic cells.

Reciprocal inhibition of Cd(2+) and Ca(2+) uptake in human intestinal crypt cells for voltage-independent Zn-activated pathways.

Cadmium-Ca-Zn interactions for uptake have been studied in human intestinal crypt cells HIEC. Our results failed to demonstrate any significant cross-inhibition between Cd and Ca uptake under single metal exposure conditions. However, they revealed a strong reciprocal inhibition for a Zn-stimulated mechanism of transport.

Effects of Cu on plasma cortisol and cortisol secretion by adrenocortical cells of rainbow trout (Oncorhynchus mykiss).

Fish are exposed to multiple stressors, often acting concurrently, in their environment. To evaluate the potential of Cu to act as a chemical stressor, rainbow trout (Oncorhynchus mykiss) were exposed to Cu (30 or 80 microg/l) for 30 days in the laboratory and they were subjected to a physical stressor (1 min air exposure) before sampling. Physiological stress indicators in the whole fish as well as cortisol secretion by adrenocortical cells in vitro were measured.

Characterization of cadmium uptake in human intestinal crypt cells HIEC in relation to inorganic metal speciation.

Cadmium (Cd) uptake was studied under inorganic exposure conditions in normal human intestinal crypt cells HIEC. The uptake time course of 0.3 microM Cd in a serum-free chloride medium was analyzed according to a first order equation with rapid initial (U0) and maximal (Umax) accumulation values of 14.

In vitro bioactivity of combustion products from 12 tobacco constituents.

Twelve chemical components of tobacco leaf, representing 50% of its dry weight, were individually combusted and the bioactivities of their combustion products i.e. total particulate matter (TPM) were assayed using three in vitro tests.

Kinetics of the early subcellular distribution of cadmium in rat hepatocytes.

The kinetics of the early subcellular distribution of cadmium (Cd) was characterized in primary cultures of rat hepatocytes exposed to 10, 50 and 100 microM Cd in a serum-free WME medium for 10, 30 or 60 min. Our results demonstrate a time- and concentration-dependent increase in Cd content with the highest metal concentration measured in the cytosol, whereas the lowest was observed in the mitochondria. With the exception of early localization in the plasma membrane, Cd concentrations in fractions were characterized by the following decreasing order of magnitude: cytosol > low density molecules approximately nuclei > lysosomes approximately mitochondria.

Different transport mechanisms for cadmium and mercury in Caco-2 cells: inhibition of Cd uptake by Hg without evidence for reciprocal effects.

Cadmium/Hg interactions have been studied in the TC7 clone of the enterocytic-like Caco-2 cells to test the hypothesis that these metals may compete for intestinal transport. Comparison of the kinetic parameter values for 203Hg(II) and 109Cd(II) uptake in a serum-free medium revealed that Hg is accumulated much more rapidly and to higher concentrations. The very rapid uptake/binding step and the initial uptake rate of 109Cd were both significantly inhibited by an excess of unlabeled Cd or Hg (apparent K(i) for Hg of 9.