Toxicity of uranium mine receiving waters to early life stage fathead minnows (Pimephales promelas) in the laboratory.

Elevated concentrations of arsenic, nickel, and molybdenum in aquatic systems around northern Saskatchewan uranium mines are an environmental concern. Early life stage fathead minnows were used to assess toxicity from several aquatic systems near the Key Lake and Rabbit Lake uranium operations. Hatching success of fish embryos exposed to waters receiving contaminants associated with uranium ore milling was reduced by 32-61% relative to controls. Mortality differed in two lakes receiving mill effluents because of opposing factors influencing metal toxicity (i.e. low pH and high hardness). In one mill receiving water (Fox Lake), larval mortality was 0%, whereas mortality was 85% in water collected from a downstream location (Unknown Lake). Fish embryos exposed to open-pit dewatering effluent receiving waters, or water from a flooded open pit (i.e. pit waters), hatched 26-39% earlier than those exposed to reference or control water. The combination of low water hardness and elevated nickel concentrations in pit waters contributed to the early hatching. Egg hatchability and hatching time were more sensitive indicators of toxicity than 'standard' endpoints, like larval mortality and growth. Current regulatory emphasis on single contaminants and standard toxicological endpoints should be re-evaluated in light of the complex interaction among confounding variables such as pH, hardness. conductivity, and multi-metal mixtures.     

Pentachlorotoluene and pentabromotoluene: results of a subacute and a subchronic toxicity study in the rat

Pentachlorotoluene (PCT) and pentabromotoluene (PBT) are environmental contaminants detected in the Great Lakes ecosystem. In view of the paucity of toxicity data and the potential for human exposure, a subacute (28 day) and a subchronic (91 day) study were conducted in the rat. In the subacute study, groups of 10 male and 10 female rats were fed the diet containing PCT or PBT at 0, 0.5, 5.0, 50 or 500 ppm for 28-days. In the subchronic study, the group size was increased to 15, the dose levels were 0, 0.05, 0.5, 5.0, 50 and 500 ppm in the diet and the exposure period was 91 days. Growth rate and food consumption were not affected by exposure to either chemical in the subacute and subchronic study. Clinical observations revealed no abnormalities. Decreased hemoglobin was observed in female rats fed 5.0 ppm PCT and higher levels in the subacute (28 day) study. In the same study the hematocrit value and erythrocyte numbers of females fed 5.0 or 500 ppm PCT diets were significantly lower than the control. In both subacute and subchronic studies mild dose-dependent histopathological changes were observed in the thyroid, liver and kidney of rats fed PCT and PBT diets. In general male rats were more susceptible than females to the treatment of PCT and PBT. Based on these data, it was concluded that the no observable adverse effect level for PCT was 50 ppm in the diet (3.5 mg/kg b.w./day) and that of PBT was 5.0 ppm (0.35 mg/kg b.w./day).     

Effects of two organophosphorus insecticides on some biochemical constituents in the nervous system and liver of rabbits

Male Baladi rabbits were acutely and sub-chronically intoxicated with cyanofenphos and profenophos. The levels of cholesterol, triglycerides, B-lipoproteins and total proteins were determined in the serum, brain, spinal cord and sciatic nerve of rabbits. Moreover, the activities of alkaline phosphatase, acid phosphatase and glutamic-pyruvic transaminase were determined in the liver of the animals. The whole studies revealed that the biochemical constituents were highly affected by the tested insecticides. Also, the liver function suffered from adverse effects of the tested insecticides.     

The influence of lindane and lindane metabolites on microsomal and mitochondrial ATPase in vitro

In vitro investigations of the influence of lindane and its metabolites were performed on microsomal and mitochondrial ATPases from liver, kidney and brain of rat and mouse. The microsomal Na+-K+-ATPases in rat liver were inhibited by the tested substances. An increase of activity was observed only with 2.5 X 10(-5) M gamma-HCH. Effects on the microsomal Na+-K+-ATPase from kidney and brain of rat were also indicated. The mitochondrial enzyme in rat liver was stimulated by all the compounds tested at concentrations of 10(-4) M - 10(-2) M. The effects on mitochondrial enzymes from kidney and brain varied in dependence on the tested substances. In the microsomes and mitochondria of mouse an influence on the Na+-K+-ATPases similar to the effects on the preparations from organs of rat was evident.     

Role of vitamin A in the haematotoxicity of hexachlorocyclohexane (HCH) in the rat.

The haematotoxicity of technical hexachlorocyclohexane (HCH) (1000 ppm) was investigated in male albino rats fed with diet free of vitamin A or containing vitamin A at 2000 or 10(5) I.U./kg. Assessment of HCH-induced haematotoxicity at the end of the 7 weeks feeding period was done on the basis of haemoglobin content, total count of red blood cells and white blood cells and the differential counts of the white blood cells as well as by parameters such as packed cell volume, mean corpuscular volume, mean corpuscular haemoglobin, mean corpuscular haemoglobin content, prothrombin time and clotting time. In the rats fed with vitamin A-free diet containing HCH, significant reductions were noticed in the total white blood cells count, clotting time and prothrombin time indicating severe haematotoxicity. Differential count of the white blood cells of these rats revealed a non-significant reduction in the lymphocyte count. The only indication of haematotoxicity caused by hexachlorocyclohexane in the vitamin A supplemented rats was a slight but statistically significant reduction of the total count of white blood cells. These results demonstrate that the haematotoxicity of hexachlorocyclohexane in the rats is enhanced by vitamin A-deficiency and its supplementation particularly in excess but not at hypervitaminotic level is protective against the toxicity.