Expression and functionality of transient receptor potential melastatin 4 (TRPM4)-like channels during development of the zebrafish.

Calcium signaling, from localized spikes to coordinated waves, are linked to cleavage, patterning, differentiation, and growth during embryonic development. The basis for control of these Ca(2+) signals is poorly defined. In this study, the expression and functionality of the transient receptor potential melastatin 4 protein (TRPM4), an ion channel that controls Ca(2+) entry into cells, was examined in the zebrafish embryo and adult.

Seasonal influences on PCB retention and biotransformation in fish.

There is extensive evidence that fish from waters with polychlorinated biphenyls (PCB)-contaminated sediments accumulate PCBs and related chemicals and that people who eat fish from contaminated waters have higher body burdens of PCBs and PCB metabolites than those who do not. PCBs and their metabolites are potentially toxic; thus, it is important to human health to understand the uptake, biotransformation, and elimination of PCBs in fish since these processes determine the extent of accumulation. The intestinal uptake of PCBs present in the diet of fish into fish tissues is a process that is influenced by the lipid composition of the diet.

Zebrafish embryos sequester and retain petrochemical combustion products: developmental and transcriptome consequences.

Zebrafish embryos are a model for studying effects of environmental stressors on development. Incomplete combustion of the environmentally relevant volatile petrochemical, 1,3-butadiene (BD) yields butadiene soot (BDS) nanoparticles, to which polynuclear aromatic hydrocarbons (PAHs) are adsorbed. In mammalian cells these PAHs are concentrated in lipid droplets and trigger up-regulation of biotransformation, oxidative stress and inflammatory genes.

Enhanced bioaccumulation of dietary contaminants in catfish with exposure to the waterborne surfactant linear alkylbenzene sulfonate.

Fish bioaccumulate a variety of contaminants and act as an exposure portal to the human consumer. Surfactants, known pharmaceutically to alter membrane permeability, change drug bioavailability and attenuate transporter function are also found in contaminant mixtures in the aquatic environment. The overall objective of this study was to determine if the surfactant C-12 linear alkylbenzene sulfonate (LAS) at environmentally relevant concentrations, alters the disposition and enhances bioaccumulation of co-exposed dietary xenobiotics in the catfish.

Influence of dietary Coexposure to benzo(a)pyrene on the biotransformation and distribution of 14C-methoxychlor in the channel catfish (Ictalurus punctatus).

Methoxychlor (MXC) is an organochlorine pesticide whose mono- and bis-demethylated metabolites, 2-(4-hydroxyphenyl)-2-(4-methoxyphenyl)-1,1,1-trichloroethane (OH-MXC) and 2,2-bis(4-hydroxyphenyl)-1,1,1-trichloroethane (HPTE), respectively, are estrogenic and antiandrogenic. Studies in vitro showed that treatment of channel catfish with a polycyclic aromatic hydrocarbon increased phase I and phase II metabolism of MXC. To determine the in vivo significance, groups of four channel catfish were treated by gavage for 6 days with 2 mg/kg (14)C-MXC alone or 2 mg/kg (14)C-MXC and 2 mg/kg benzo(a)pyrene (BaP).

Rhodamine 123 permeability through the catfish intestinal wall: Relationship to thermal acclimation and acute temperature change.

Temperature is known to influence xenobiotic retention in fish. The effect of acute and acclimatory temperature change upon Rhodamine 123 (Rho123) permeability through an in vitro catfish multi-segment (3) everted sac intestinal wall model was examined in a 9 cell matrix of acclimation and assay temperatures (10, 20 and 30 degrees C). Changes in Rho123 permeability were examined in context with membrane fluidity, xenobiotic solubility and intestinal morphology.

Demethylation of the pesticide methoxychlor in liver and intestine from untreated, methoxychlor-treated, and 3-methylcholanthrene-treated channel catfish (Ictalurus punctatus): evidence for roles of CYP1 and CYP3A family isozymes.

Exposure to the organochlorine pesticide methoxychlor (MXC) is associated with endocrine disruption in several species through biotransformation to mono-desmethyl-MXC (OH-MXC) and bis-desmethyl-MXC (HPTE), which interact with estrogen receptors. The biotransformation of [14C]methoxychlor was examined in channel catfish (Ictalurus punctatus), a freshwater species found in the southern United States. Hepatic microsomes formed OH-MXC and HPTE, assessed by comigration with authentic standards.

Intestinal bioavailability and biotransformation of 3,3',4,4'-tetrachlorobiphenyl (CB 77) in in situ preparations of channel catfish following dietary induction of CYP1A.

Previous studies with the catfish in situ perfused intestinal preparation have demonstrated a significant decline in the intestinal bioavailability of a coplanar polychlorinated biphenyl (PCB), 3,3',4,4'-tetrachlorobiphenyl (CB 77)(14C-TCB) dose in animals pre-exposed in vivo to TCB. This response was accompanied by CYP1A induction in the intestine, but little effect upon the oxidative metabolism of the subsequent in situ dose of [14C]-TCB. To ascertain the basis of these responses and the intestine specific contributions, the intestinal bioavailability and metabolism of [14C]-TCB were examined in the in situ intestinal preparation following in vivo exposure to beta-naphthoflavone (BNF; 0, 10 or 50 mg BNF/kg diet for 10 days), BNF was selected as a known inducer of CYP1A and as a compound with a structure unlikely to influence or directly partake in diffusion based TCB concentration gradients.

Increased toxicity of benzo(a)pyrene-7,8-dihydrodiol in the presence of polychlorobiphenylols.

Benzo(a)pyrene (BaP) and polychlorinated biphenyls (PCBs) often co-exist in contaminated environments. Polychlorobiphenylols (OH-PCBs), formed by CYP-dependent monooxygenation of PCBs, are potent inhibitors of the glucuronidation of hydroxylated BaP metabolites. We hypothesized that OH-PCBs could drive the biotransformation of (-)BaP-7,8-dihydrodiol (BaP-7, 8-D) away from detoxication and towards formation of the reactive metabolite.