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Aquatic species can be exposed to endocrine disrupting chemicals (EDCs) in wastewater that often includes the weak estrogen, 4-nonylphenol (NP) and the potent estrogen, 17alpha-ethinylestradiol (EE). The goal of the present study was to determine concentration-dependent effects of developmental exposure to NP and EE on gametogenesis, as well as gonad,(More)
1. Smooth muscle contraction is activated primarily by the Ca2+-calmodulin (CaM)-dependent phosphorylation of the 20 kDa light chains (LC20) of myosin. Activation can also occur in some instances without a change in intracellular free [Ca2+] or indeed in a Ca2+-independent manner. These signalling pathways often involve inhibition of myosin light chain(More)
Increasing evidence suggests that sublethal effects of natural or xenobiotic chemicals in the environment may be mediated via the stimulation of apoptosis. To investigate whether apoptosis can be induced in fish by weakly estrogenic and androgenic chemicals, adult male Japanese medaka (Oryzias latipes) were exposed to 100 ppb of the estrogenic alkylphenol,(More)
TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) remains a potent and persistent toxicant in aquatic environments, causing lethal developmental deformities in fish. However, few studies have examined sublethal or persistent effects of developmental TCDD exposure and none have examined its effects on swimming capabilities in sub-adult fish. The objective of the(More)
Cytochrome P4501A (CYP1A) and the 70-kDa stress protein (HSP70) were determined using Western blotting in the ovary and liver of juvenile female rainbow trout (Oncorhynchus mykiss) exposed for 4 days to beta-naphthoflavone (betaNF) following a single intraperitoneal injection. Ovarian CYP1A protein was observed in both control and betaNF-exposed fish,(More)
Developmental exposure to aryl hydrocarbon receptor (AhR) agonists in fish causes severe defects in the cardiovascular system. However, the effects of acute AhR agonist exposure on the adult fish cardiovascular system are not clear. We hypothesized that AhR-mediated changes in adult vascular tissue gene expression would differ from that of hepatic tissue.(More)
Hyperglycemia produces oxidative stress, which may impair endothelial function. Methylglyoxal, a reactive intermediate metabolite of glucose, is known to cause oxidative stress and is produced when excess carbohydrate is consumed in diabetic patients, but postprandial responses in healthy patients are unknown. We hypothesize that methylglyoxal levels will(More)
While swimming endurance (critical swimming speed or U(crit)) and lipid stores have both been reported to acutely decrease after exposure to a variety of toxicants, the relationship between these endpoints has not been clearly established. In order to examine these relationships, adult zebrafish (Danio rerio) were aqueously exposed to solvent control(More)
Sublethal effects observed in fish exposed to environmental estrogens may be mediated via stimulation of cell death. To investigate whether cell death is induced in fish after chronic exposure to estrogenic chemicals, Japanese medaka (Oryzias latipes) were exposed from hatch until sexual maturity to 10 ng/L 17alpha-ethinylestradiol (EE2) or acetone solvent(More)
Previous studies from this laboratory have demonstrated an enhancement in both the contractile and signaling response to stimulation of either alpha-1 adrenoceptors or guanine nucleotide binding proteins (G proteins) in arteries from male Wistar rats with 12 to 14 weeks of streptozotocin-induced diabetes. The purpose of the present investigation was to(More)