No description available.

No description available.

Digitized by Kansas State University Libraries

Digitized by Kansas State University Libraries

Seven prospective biological indicators of systemic toxicity were examined at time points ranging from 15 minutes to 24 hours using male Sprague-Dawley rats, B6C3F1 mice, Golden-Syrian hamsters and Hartley guinea pigs following intraperitoneal dosing with 0.1 mg/kg and 1.0 mg/kg sodium arsenite. Rats and mice were also dosed with 1.0 mg/kg sodium arsenate. Pyruvate dehydrogenase (PDH) activity was significantly depressed at early time points in mice, hamsters and guinea pigs and at later time points in rats dosed with arsenic (III). Rats and mice dosed with arsenic (V) also exhibited PDH depression at early time points. Uroporphyrin and coproporphyrin excretion was elevated in mice following arsenic (III) dosing. Coproporphyrin excretion was elevated in rats following arsenic (V) dosing. Blood glucose, creatinine, urea nitrogen and creatinine were unchanged by arsenic dosing. Based upon the amount and types of biological responses observed, the mouse appears to be the most sensitive animal model for the further study of arsenic toxicity.

<p> Endocrine disrupting chemicals are a group of exogenous compounds which disrupt the endocrine functions of human and wildlife. This disruption might be in the synthesis, storage, release, and actions of specific hormones. Endocrine disrupting chemicals encompass a variety of chemical classes including drugs, compounds used in plastic consumer products manufacturing, pollutants, insecticides, herbicides, and even naturally-occurring botanical products like phytoestrogens. Most of these disrupters produce estrogenic properties because of having structural similarity to endogenous 17 beta estradiol. Mimicking estradiol, they can interfere with its actions resulting in the development of several diseases, such as nervous system, diabetes, obesity, breast cancers, and reproductive impairments. One of the endocrine disrupting chemicals of most interest is bisphenol A. </p><p> Bisphenol A is a carbon-based synthetic compound and it is used in epoxy resins, polycarbonate plastics, fungicides, antioxidants, stabilizers in rubber, and as a component of dental sealants. Numerous studies have found that bisphenol A may accidentally leak into canned foods or plastic bottled drinks ingested by humans. Studies indicate that bisphenol A effects are due to its estrogenic activity and the ability to bind and activate the estrogen receptor specifically. A growing number of studies have indicated that bisphenol A might be responsible for reduction in sperm count, spermatogenesis, aromatase, seminal fluid, 17 beta hydroxysteroid dehydrogenase activity, and testosterone biosynthesis. The primary objective of this capstone project is to review the available literature in order to determine the mechanism of bisphenol A action on testosterone biosynthesis. The working hypothesis was that bisphenol A-induced reduction in testosterone production may be due predominantly to inhibition of 17 beta beta hydroxysteroid dehydrogenase rather than an increase in aromatase enzyme activity. This study had the following specific aims: 1) review the sex steroid biosynthesis pathway, 2) review the endocrine disrupting chemicals; 3) determine a mechanism by which bisphenol A mimics estrogen and affects testosterone synthesis. Literature review was conducted using the databases PubMed, Ovid Medline, CINAHL Plus, as well as the search engine Google Scholar for the period 1940 to present. The keywords used: bisphenol A, testosterone, luteinizing hormone, 17 beta hydroxysteriod dehydrogenase enzymes. It was found that human studies were limited to urine measurements in which increased bisphenol A correlated with decreased sperm account and seminal fluid volume. In animal studies, bisphenol A reduced testosterone production by direct action on the leydig cells. In the ovarian granulosa cells, bisphenol A reduced aromatase enzyme activity but unlikely to be the method, in the testes as, a decrease in aromatase activity would cause an increase in testosterone level. Since bisphenol A causes significant decrease in testosterone biosynthesis, this suggests that the inhibition of 17 beta hydroxysteroid dehydrogenase, the enzyme that converts androstenedione to testosterone, is probably the principal target for bisphenol A. In conclusion, the literature supports a strong threat from bisphenol A on male reproductive function and every action must be taken seriously to reduce the exposure of male to this endocrine disrupting chemical. </p>

Road runoff contains a complex mixture of contaminants including metals, anions, and hydrocarbons. This runoff discharges into natural water courses which are often small streams. The concentration of these chemicals in the drainage water and receiving stream depends on a number of site specific characteristics such as traffic volume, area of road drained and size of the stream. It was postulated that these pollutants have a deleterious affect on macroinvertebrate community structure which would result in subsequent effects on macroinvertebrate function (i. e. litter processing). Further, it was hypothesised that impacts would be greatest in small streams, receiving drainage waters from large areas of heavily used motorway and that only a limited number of chemicals would be responsible for any effects. Field surveys demonstrated that macroinvertebrate community structure and function was impacted at one of the three sites studied, namely Pigeon Bridge Brook. The downstream station at this site received motorway runoff drainage from the largest area of road surface, was the smallest stream and had the highest metal and hydrocarbon concentrations in both stream water and sediments (Maltby et al., 1995a). Macroinvertebrate species richness and diversity were significantly reduced below the discharge. Species generally considered 'sensitive' to pollutants such as stoneflies, gammarids, molluscs and trichopterans were reduced in relative abundance whilst more 'tolerant' opportunistic species such as chironomids and tubificid worms increased in relative abundance downstream of the discharge. An assessment of the trophic composition of the community (i. e. functional feeding groups) indicated that there was a differential loss of functional groups, with significantly lower relative abundances of shredders and scrapers and an increase in collectors downstream of the motorway discharge. The changes in both the structure and trophic biology of the macroinvertebrate community resulted in a significant reduction in macroinvertebratemediated leaf processing downstream of the motorway discharge. Although field surveys indicated macroinvertebrate community structure and function were negatively impacted below the motorway discharge at Pigeon Bridge Brook they cannot establish causal relationships. In-situ and laboratory studies were therefore performed to address the mechanistic basis for the impact. In-situ and laboratory lethality exposures did not fully explain the field distribution of the species used in toxicological studies; Gammarus pulex (L. ), Nemoura cinerea (Retz. ), Potamopyrgus jenkinsi (Smith), Chironomus riparius (Meigen) and Tubifex tubifex (Müller). In acute lethality tests stream water from Pigeon Bridge Brook was not toxic to any of the species. In contrast, G. pulex and N. cinerea showed slight, but significant mortality when exposed to downstream sediment from this site. Sediment manipulation and sediment solvent and acid extract exposures indicated that the solvent extractable fraction of the sediment was responsible for this toxicity to G. pulex but not to N. cinerea. These results indicated that aromatic hydrocarbons in the sediment may be responsible for the toxicity and this has subsequently been shown to be the case (Maltby et al., 1995b). ifi Since lethality studies did not fully explain field -distributions of the animals sub-lethal toxicity avoidance behaviour tests were employed using sediment, manipulated sediments and sediment extracts. The sensitivity to downstream field sediment, indicated by avoidance decreased in the order P. jenkinsi > G. pulex > C. riparius> T. tubifex = N. cinerea and to a solvent extract of this sediment in the order G. pulex > P. jenkinsi > C. riparius > N. cinerea > T. tubifex. Acid sediment extracts and solvent extracted sediments induced no avoidance responses in these animals. Gammarus pulex was thought to be the dominant shredding macroinvertebrate at Pigeon Bridge Brook. Reductions in macroinvertebrate-mediated leaf processing could therefore be the result of sub-lethal effects of motorway contamination on the feeding activity of this species. In-situ exposures indicated that the consumption of leaf material by G. pulex was reduced at the downstream station and laboratory exposures indicated this was principally a result of sediment toxicity. Sediment extract exposures indicated that the solvent extractable fraction was again responsible for the majority of this effect. Accumulation of metals and aromatic hydrocarbons on the leaf material had very little effect on leaf consumption or choice. However, reduced colonisation of leaf material by aquatic hyphomycetes reduced both leaf choice and consumption when the material was conditioned at the downstream station. The major uptake route of aromatic hydrocarbons by G. pulex was via aqueous sources and not from food. In conclusion motorway derived contamination in small streams has both lethal and sublethal effects on some macroinvertebrates. This affects macroinvertebrate structural and trophic characteristics which subsequently have a deleterious effect on important ecosystem functions.

No description available.

No description available.

No description available.