80 papers published between 1970 and 1984 were evaluated for results pertaining to chemical-induced aneuploidy in mammalian male germ cells. Diverse assays and end points were represented. The assays considered to involve direct measures of aneuploidy were based upon chromosome counts in premeiotic, meiotic, and embryonic cells, and the male pronucleus, or upon phenotypic expression of X-linked genetic markers. Assays in which indirect measures were interpreted as evidence for aneuploidy included those primarily assessing chiasma frequencies, univalent frequencies, and spermatid/sperm sex chromosome body counts. An initial screening to reject studies with insufficient data and those which did not involve a single chemical test agent led to the elimination of 39 papers from further review. The remaining 41 papers reported effects from 46 different chemicals. These papers were rigorously assessed for adequacy of experimental protocols, relevance of end points as direct measures of aneuploidy, and completeness of data presentation and statistical analysis. Criteria specific to each assay were also considered. 4 chemical tests were considered to provide reliable positive or negative aneuploidy data. Cyclophosphamide and chloral hydrate each caused metaphase II hyperploidy when injected into mice. Very limited analyses of trenimon and isoniazid provided negative results. Test findings for 44 chemicals were viewed as inconclusive. It was concluded that standardization of tests to evaluate chemical-induced aneuploidy in male germ cells and the application of these tests towards increasing the data base are badly needed.

Aneuploidy↗

PubMedDate not supplied

Spermatid micronucleus analyses of trichloroethylene and chloral hydrate effects in mice.

Mice were exposed by inhalation to trichloroethylene (TCE) or by i.p. injection to the TCE metabolite, chloral hydrate (CH). Early spermatids were analyzed for micronucleus (MN) frequency and the presence or absence of kinetochore(s) using fluorochrome-labeled anti-kinetochore antibodies. It was determined that 5 consecutive days of exposure to 5, 50 or 500 ppm TCE during preleptotene through early pachytene stages of meiotic cell development do not result in increased frequencies of spermatid MN. CH at 41, 83 or 165 mg/kg was positive for spermatid MN induction when treatments corresponded to spermatogonial stem cell or preleptotene spermatocyte stages of development; negative results were obtained after treatments of leptotene-zygotene or diakinesis-metaphase stages. The significantly increased levels of MN observed were invariably of the kinetochore-negative type.

Aneuploidy↗

PubMedDate not supplied

Methylmercury alters glutamate transport in astrocytes.

Methylmercury (MeHg) is a significant environmental contaminant that will continue to pose great risk to human health. Considerable attention in the scientific and health policy fora is focused on the question of whether MeHg intake from a diet high in fish is associated with aberrant CNS function. A number of recent studies (Kjellstrom et al., 1986: Kjellstrom, T., Kennedy, P., Wallis, S., Mantell, C., 1986. Physical and mental development of children with prenatal exposure to mercury from fish. Stage I: preliminary tests at age 4. Solna, Sweden. National Swedish Environmental Protection Board Report 3080, 1989: Kjellstrom, T., Kennedy, P., Wallis, S., Stewart, A., Friberg, L. et al., 1989. Physical and mental development of children with prenatal exposure to mercury from fish. Stage II: interviews and psychological tests at age 6. Solna, Sweden. National Swedish Environmental Protection Board Report 3642; McKeown-Eyssen et al., 1983: McKeown-Eyssen, G., Ruedy, J., Neims, A. , 1983. Methylmercury exposure in Northern Quebec II: neurologic findings in children. American Journal of Epidemiology 118, 470-479; Grandjean et al., 1997: Grandjean, P., Weihe, P., White, R. F., Debes, F., Araki, S., Yokoyama, K., Murata, K., Sorensen, N., Dahl, R., Jorgensen, P. J., 1997. Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury. Neurotoxicology and Teratology 19, 417-428) suggest that fetal exposure at levels attained by mothers eating fish regularly during pregnancy are associated with neurological deficits in their offspring. Astrocytes play a key role in MeHg-induced excitotoxicity. (1) MeHg preferentially accumulates in astrocytes. (2) MeHg potently and specifically inhibits glutamate uptake in astrocytes. (3) Neuronal dysfunction is secondary to disturbances in astrocytes. (4) Co-application of nontoxic concentrations of MeHg and glutamate leads to the typical appearance of neuronal lesions associated with excitotoxic stimulation. (5) MeHg induces swelling of astrocytes. These observations are fully consistent with MeHg-induced dysregulation of excitatory amino acid homeostasis, and indicate that a glutamate-mediated excitotoxic mechanism is involved. This manuscript details the role of astrocytes in mediating MeHg-induced excitotoxicity, and elaborates on the protective role afforded by metallothioneins (MTs) in attenuating MeHg cytotoxicity.

Animals↗

PubMedDate not supplied

A private inquiry into the circumstances surrounding the 1972 death of John Gomilla, Jr., who died after allegedly consuming ten hallucinogenic mushrooms while residing in Hawaii.

In December 1972, an 18-year-old male apparently took an accidental overdose of heroin. After becoming ill, he attempted to receive treatment for his condition by being admitted to the emergency room of Wahiawa General Hospital. When confronted by attending physicians in the emergency room as to the nature of his illness, the youth stated that he had only eaten 10 hallucinogenic mushrooms (an average dose for Copelandia cyanescens, the mushroom in question) and nothing else. This story was most likely concocted either by the youth himself or by some of his friends, who probably thought that they could or would be prosecuted for the use of an illegal substance. It is not uncommon that when confronted by an overdose of drugs, many young people are afraid to report their illness to the proper medical authorities out of fear of prosecution due to their illegal activities (Young et al. 1982). The doctors who attempted to treat this young man should not be held liable for his death, even though their treatment of the patient was more supportive (i.e., the talk-down method) than pharmacological. They had no way of knowing that the patient had lied to them about his condition. While it is true that several doctors had diagnosed Gomilla as possibly suffering from muscarine poisoning, why was no atropine or scopolamine administered to the patient? And why was his stomach not pumped and specimens collected for a toxicologist to study for the presence of toxins?(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMedDate not supplied

An ethnomycological review of psychoactive agarics in Australia and New Zealand.

A comprehensive review is presented of the recreational and accidental ingestion of psychoactive mushrooms in Australia and New Zealand; 15 recognized species are considered from Australia and eight from New Zealand. Common epithets, potency levels, and methods of ingestion are discussed. Legal aspects involving the use of these psychoactive fungi are noted. In addition, medical and psychoactive effects of these mushrooms and treatment for psilocybian mushroom poisoning are described. Numerous case reports, with commentary, are also presented.

Australia↗

PubMedDate not supplied

Male fertility, sister chromatid exchange, and germ cell toxicity following exposure to mixtures of chlorinated phenoxy acids containing 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Fertility and sperm number, motility, and morphology were analyzed in male C57BL/6 mice exposed to various mixtures of 2,4-dichlorophenoxyacetic acid (2,4-D), 2,4,5-trichlor-ophenoxyacetic acid (2,4,5-T), and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the diet for 8 wk. Somatic cell (bone marrow) sister chromatid exchange frequencies were also evaluated in mice injected with similar chemical mixtures. The concentration of the test chemicals was such that the average daily feeding dose in the three mixtures or control was 40 mg/kg 2, 4-D, 40 mg/kg 2,4,5-T, and 2.4 micrograms/kg TCDD; 40 mg/kg 2,4-D, 40 mg/kg 2,4,5-T and 0.16 microgram/kg TCDD; 20 mg/kg 2, 4-D, 20 mg/kg 2,4,5-T, and 1.2 micrograms/kg TCDD; or no chemical added (control). No significant dose-related effects were observed in the treated mice compared to the control group.

2,4,5-Trichlorophenoxyacetic Acid↗