The pyrethroid insecticide, bifenthrin, is frequently measured at concentrations exceeding those that induce acute and chronic toxicity to several invertebrate and fish species residing in the Sacramento-San Joaquin Delta of California. Since the brain is considered to be a significant target for bifenthrin toxicity, juvenile steelhead trout (Oncorhynchus mykiss) were treated with concentrations of bifenthrin found prior to (60 ng/L) and following (120 ng/L) major stormwater runoff events with nontargeted metabolomics used to target transcriptomic alterations in steelhead brains following exposure. Predicted responses were involved in cellular apoptosis and necrosis in steelhead treated with 60 ng/L bifenthrin using the software Ingenuity Pathway Analysis. These responses were predominately driven by decreased levels of acetyl-L-carnitine (ALC), docosahexaenoic acid (DHA), and adenine. Steelhead treated with 120 ng/L bifenthrin had reductions of lysophosphatidylcholines (LPC), lysophosphatidylethanolamines (LPE), and increased levels of betaine, which were predicted to induce an inflammatory response. Several genes predicted to be involved in apoptotic (caspase3 and nrf 2) and inflammatory (miox) pathways had altered expression following exposure to bifenthrin. There was a significantly increased expression of caspase3 and miox in fish treated with 120 ng/L bifenthrin with a significant reduction of nrf 2 in fish treated with 60 ng/L bifenthrin. These data indicate that bifenthrin may have multiple targets within the brain that affect general neuron viability, function, and signaling potentially through alterations in signaling fatty acids.
Bisphenol
S (BPS), an alternative for bisphenol A (BPA) that is present in thermal
paper and numerous consumer products, has been linked to estrogenic,
cytotoxic, genotoxic, neurotoxic, and immunotoxic responses. However,
the mechanisms of BPS toxicity remain poorly understood. Here, following
exposure to environmentally relevant concentrations ranging from 0.1
to 100 μg/L BPS, transcriptional changes evaluated by enriched
gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG),
and Ingenuity Pathway Analysis (IPA) predicted cardiac disease and
impairment of immune function in zebrafish at the embryo-to-larvae
stage. Consistent with impacts predicted by transcriptional changes,
significant sublethal impacts were observed ranging from reduced heart
rate [8.7 ± 2.4% reductions at 100 μg/L BPS treatment; P < 0.05] to abnormal cardiac morphology [atrial/ventricle
area significantly increased; 36.2 ± 9.6% at 100 μg/L BPS
treatment; P < 0.05]. RNA-sequencing analysis
results also indicated changes in nitric oxide synthetase (NOS2) and
interleukin 12 (IL12) after BPS treatment, which was confirmed at
the protein level. Increased expression of other cytokine genes was
observed in larvae, suggesting inflammatory responses may be contributing
to cardiac impairment by BPS. BPS caused cardiotoxicity, which temporally
corresponded with inflammatory responses as predicted from RNA sequencing
and confirmed at the protein and cellular levels of biological organization.
Additional study is needed to find causal linkages between these responses.
Formation of halogenated disinfection byproducts (DBPs) from pharmaceutically active compounds has been observed in water supply systems following wastewater chlorination. Although research has been limited thus far, several studies have shown that halogenated DBPs may elicit increased toxicity compared to their parent compounds. For example, the lipid regulator gemfibrozil has been shown to form chlorogemfibrozil (Cl-gemfibrozil) and bromogemfibrozil (Br-gemfibrozil) following chlorination, which are more potent antiandrogens in male Japanese medaka (Oryzias latipes) compared to their parent compounds. In the present study, we aimed to characterize the bioaccumulative ability of halogenated gemfibrozil DBPs in marine polychaetes via chronic sediment exposures and, consequently, to assess the chronic and acute toxicity of halogenated gemfibrozil DBPs through sediment (in vivo) and aqueous (in vivo and in silico) toxicity evaluations. Following 28 day sediment exposures, Cl-gemfibrozil and Br-gemfibrozil bioaccumulated within Neanthes arenaceodentata, with both compounds reducing survival and growth. The biota−sediment accumulation factors determined for Clgemfibrozil and Br-gemfibrozil were 2.59 and 6.86, respectively. Furthermore, aqueous 96 h toxicity tests with N. arenaceodentata indicated that gemfibrozil DBPs elicited increased toxicity compared to the parent compound. While gemfibrozil had an acute LC50 value of 469.85 ± 0.096 mg/L, Cl-gemfibrozil and Br-gemfibrozil had LC50 values of 12.34 ± 0.085 and 9.54 ± 0.086 mg/L, respectively. Although acute toxicity is relatively low, our results indicate that halogenated gemfibrozil DBPs are bioaccumulative and may elicit effects in apex food web organisms prone to accumulation following lifelong exposures.
Crude
oil-derived polycyclic aromatic hydrocarbons (PAHs) are pervasive
environmental pollutants with well-established detrimental effects
on the health of marine organisms. Following large-scale oil spills
in the marine environment, there is a critical need for noninvasive
sampling methods to assess environmental exposure to PAHs without
further perturbations to the population and for long-term monitoring
following a spill. To test the efficacy of epidermal mucus mRNA as
a source for noninvasive sampling, juvenile mahi-mahi (Coryphaena
hippurus, ∼28 days of age) were exposed to control
seawater or two concentrations of high-energy water accommodated fractions
(HEWAFs; 5% or 10%) of Deepwater Horizon surface
oil for 48 h. Whole-transcriptome sequencing revealed differential
expression of 501 transcripts in the low-HEWAF exposure (∑PAH
= 16.55 μg/L) and 196 transcripts in the high-HEWAF exposure
(∑PAH = 23.03 μg/L), suggesting differential regulation
of mRNA in mucus following PAH exposure. In addition to differential
expression of well-established biomarkers of PAH exposure such as
cytochrome P450 enzymes, the mucosal transcriptome showed differential
expression of transcripts involved in immune response, cardiotoxicity,
and calcium homeostasis that parallel molecular responses in whole
embryos. The consistency of the changes in expression in the epidermal
mucus compared to that of tissues obtained from lethal sampling suggests
that mucus is a promising source for noninvasive monitoring techniques.
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