The sensitivity of wild rice (Zizania palustris) to sulfide is not well understood. Because sulfate in surface waters is reduced to sulfide by anaerobic bacteria in sediments and historical information indicated that 10 mg/L sulfate in Minnesota (USA) surface water reduced Z. palustris abundance, the Minnesota Pollution Control Agency established 10 mg/L sulfate as a water quality criterion in 1973. A 21-d daily-renewal hydroponic study was conducted to evaluate sulfide toxicity to wild rice and the potential mitigation of sulfide toxicity by iron (Fe). The hydroponic design used hypoxic test media for seed and root exposure and aerobic headspace for the vegetative portion of the plant. Test concentrations were 0.3, 1.6, 3.1, 7.8, and 12.5 mg/L sulfide in test media with 0.8, 2.8, and 10.8 mg/L total Fe used to evaluate the impact of iron on sulfide toxicity. Visual assessments (i.e., no plants harvested) of seed activation, mesocotyl emergence, seedling survival, and phytoxicity were conducted 10 d after dark-phase exposure. Each treatment was also evaluated for time to 30% emergence (ET30), total plant biomass, root and shoot lengths, and signs of phytotoxicity at study conclusion (21 d). The results indicate that exposure of developing wild rice to sulfide at ≥3.1 mg sulfide/L in the presence of 0.8 mg/L Fe reduced mesocotyl emergence. Sulfide toxicity was mitigated by the addition of Fe at 2.8 mg/L and 10.8 mg/L relative to the control value of 0.8 mg Fe/L, demonstrating the importance of iron in mitigating sulfide toxicity to wild rice. Ultimately, determination of site-specific sulfate criteria taking into account factors that alter toxicity, including sediment Fe and organic carbon, are necessary. Environ Toxicol Chem 2017;36:2217-2226. © 2017 SETAC.
The potential reproductive and endocrine toxicity of boric acid (BA) in the African clawed frog, Xenopus laevis, was evaluated using a 30-day exposure of adult frogs. Adult female and male frogs established as breeders were exposed to a culture water control and 4 target (nominal) test concentrations [5.0, 7.5, 10.0, and 15 mg boron (B)/L, equivalent to 28.5, 42.8, 57.0, and 85.5 mg BA/L] using flow-through diluter exposure system. The primary endpoints measured were adult survival, growth (weight and snout-vent length [SVL]), necropsy data, reproductive fecundity, and development of progeny (F1) from the exposed frogs. Necropsy endpoints included gonad weight, gonado-somatic index (GSI), ovary profile (oocyte normalcy and stage distribution), sperm count, and dysmorphology. Endocrine endpoints included plasma estradiol (E2), testosterone (T), dihydrotestosteone (DHT), gonadal CYP 19 (aromatase), and gonadal 5α-reductase (5-AR). BA exposure to adult female X. laevis increased the proportion of immature oocytes (< stage II) in the ovaries of females, reduced sperm counts and increased sperm cell dysmorphology frequency in male frogs exposed to 15 mg B/L. No effects on the other general, developmental (F1), or endocrine endpoints were observed. Based on the results of the present study, the no observed adverse effects concentration (NOAEC) for the reproductive endpoints was 10 mg B/L; and 15 mg B/L for reproductive fecundity, F1 embryo larval development, and endocrine function. These results confirmed that although BA is capable of inducing reproductive toxicity at high concentrations, it is not an endocrine disrupting agent.
The impacts of contaminated sediment from 2 ponds in Bermuda on immune function in newly metamorphosed cane toads were examined. In the present study, a partial life-cycle experiment exposing Gosner stage 20 cane toad tadpoles to pond sediment and laboratory culture water through metamorphosis and into a juvenile state was performed. A basic immunology battery, including general necropsy, spleen somatic index, spleen white pulp content, splenocyte tissue density, and splenocyte viability, was conducted in newly metamorphosed Rhinella marina exposed to Bermuda freshwater sediment and baseline specimens collected from 2 separate populations in south Texas and south Florida, USA. Immune function was evaluated using a lymphocyte proliferation assay with subset specimens infected with Mycobacterium chelonae. In the Bermuda population exposed to pond sediment, splenocyte tissue density was markedly lower and lymphocyte proliferation substantially less relative to cohorts exposed to control sediment and to the North American populations. Considerable increases in spleen weight and liver and spleen lesions related to M. chelonae infection were recorded in challenged Bermuda R. marina compared with unchallenged specimens. Overall, immune function in Bermuda R. marina was compromised compared with North American mainland R. marina regardless of treatment but more dramatically in specimens exposed to Bermuda pond sediments. Environ Toxicol Chem 2016;35:2604-2612. © 2016 SETAC.
The impact of the perfluoro‐chemical, perfluorooctanesulfonate (PFOS), on gonadal steroidogenesis during sexual differentiation in Silurana tropicalis was examined because of its ubiquity in the environment, bioaccumulative nature and potential to disturb endocrine activity. A partial life cycle study exposing S. tropicalis to varying concentrations of PFOS 0.06, 0.13, 0.25, 0.50 and 1.0 mg PFOS/L [nominal]) was conducted. Gonad and plasma samples were collected from juvenile control specimens and organisms exposed to PFOS from early embryo through 150 days post‐metamorphosis. Gonad CYP17, aromatase and 5α‐reductase activities were measured. Plasma estradiol, testosterone, dihydrotestosterone (DHT) and gonadal testosterone were measured in both males and females. Increased plasma DHT and gonadal testosterone were found in PFOS‐treated juvenile male S. tropicalis compared to controls. Decreased plasma estradiol, but not testosterone, was detected in PFOS‐treated female S. tropicalis compared to controls. Plasma DHT was not detected and an increase in gonadal testosterone was detected in PFOS‐treated female frogs. Female S. tropicalis exposed to PFOS exhibited a concentration‐related decrease in the mean aromatase activity, but not 5α‐reductase. PFOS exposure in male frogs induced a concentration‐related increase in 5α‐reductase activity, but did not alter aromatase activity compared to control frogs. A concentration‐related increase in CYP 17,20‐lyase activity, but not 17‐hydroxylase activity, was found in both female and male S. tropicalis exposed to PFOS.
Relapse poses a significant barrier to the development of effective treatments for substance use disorder (SUD). Cue‐induced drug craving increases during drug abstinence, potentially affecting the efficacy of treatments for SUD. Disruptions in glutamatergic signaling are characteristic of SUDs. Glutamate is maintained by a combination of astrocytic and neuronal transporters within the nucleus accumbens (ACb) and disruptions in this homeostasis engender SUD. One transporter, the cysteine‐glutamate transporter (xCT), is primarily localized on astrocytes and helps maintain glutamate concentrations. This process is disrupted by cocaine use, leading to increased cue‐induced craving. The therapeutic N‐acetylcysteine (NAC) lowers cue‐induced relapse to cocaine. However, little research has shown how these effects extend to other psychostimulants, such as amphetamine (AMP). Though both are psychostimulants, AMP and cocaine have distinct mechanisms of action in the brain, particularly with regards to dopamine neurotransmission. In the present study, we assessed disruption of astrocytes and xCT expression following AMP self‐administration (SA). We also assessed the degree to which disruptions in astrocyte or xCT expression might explain an increased propensity for relapse when presented with drug cues and the degree to which NAC can attenuate relapse. 78 male Sprague‐Dawley rats were surgically implanted with jugular catheter to allow for intravenous SA of AMP. Upon recovery, all rats underwent 14, 2‐hr fixed‐ratio‐1 SA sessions for AMP or the saline (SAL) control. Active lever presses resulted in an infusion of amphetamine (0.1 mg/kg/infusion) which was followed by a 20 s time‐out period signaled by the illumination of both cue lights. After 14 SA sessions, all rats entered a forced abstinence period where they were not exposed to the drug or drug‐related cues. During abstinence, all rats were given daily injections of NAC (100 mg/mL/ip) or the saline vehicle. Cue‐induced relapse tests were conducted at the cessation of the abstinence period. During the relapse test, active lever presses resulted in the illumination of the cue lights present during SA testing, but no delivery of the drug itself. One subset of rats underwent relapse testing after one withdrawal day (WD) 1 and one subset underwent testing on WD 14 to examine any increases in relapse. Following testing, all rats were perfused and brains were extracted for immunofluorescence (IF) analysis of astrocyte and xCT transporter expression within the ACb and medial prefrontal cortex using a simultaneous immunofluorescence (IF) method. During the cue‐induced relapse test, cue‐induced responding was significantly higher in AMP‐treated rats compared to SAL‐treated rats. Importantly, NAC failed to attenuate relapse at either WD 1 or WD 14. We hypothesized that xCT expression would remain unaltered between WD 1 and WD 14 for rats treated with NAC. However, given that NAC failed to lower relapse at either time point, IF results will help determine inform the inefficacy of...
The impact of the brominated flame-retardant mixture, DE-71, on gonadal steroidogenesis during sexual differentiation in Silurana tropicalis was examined. A partial lifecycle study exposing S. tropicalis to varying concentrations of DE-71 (0.0, 0.65, 1.3, 2.5, and 5.0 μg/l [nominal]) was conducted from early gastrula-stage embryo to 150 days postmetamorphosis (dpm). Exposure of S. tropicalis to DE-71 induced liver necrosis and induced abnormal ovary development characterized by previtellogenic oocyte necrosis and arrested development of vitellogenic oocytes in females in a concentration-dependent manner. Decreased mean plasma dihydrotestosterone (DHT) and T, gonad T, and increased mean plasma E2 levels were found in 150 dpm DE-71-treated male S. tropicalis compared to controls. Plasma E2 levels in females were not significantly altered compared to control S. tropicalis, although lower plasma and gonad T were detected. Mean gonadal CYP 19 aromatase activity in both male and female S. tropicalis exposed to DE-71 was not appreciably affected. Decreased mean male 5α-reductase and CYP17 activities in both male and females were observed compared to control frogs. Overall, these studies suggested that PBDE exposure induced liver necrosis and abnormal ovary development; and reduced circulating and gonadal androgens resulting in a phenotypic skew in sex ratio toward the female sex in S. tropicalis.
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