Mammalian exposure

Toxic effects of nickel to humans and laboratory mammals are documented for respiratory, cardiovascular, gastrointestinal, hematological, musculoskeletal, hepatic, renal, dermal, ocular, immunological, developmental, neurological, and reproductive systems. Nickel toxicity in mammals is governed by the chemical form of nickel, dose, and route of exposure. Mammalian exposure to nickel by inhalation or cutaneous contact was more significant than oral exposure. To protect humans and other mammals against respiratory effects, proposed air-quality criteria are 0.01 to less than... 

Modulation of the Killing of Mammalian Cells by Thiols. Important aspects of the effects of exogenous thiols on clonogenic cell survival following exposure to low linear energy transfer (LET) radiations include the following. 

Calcium is readily abundant in the mammalian diet. A 70 kg human contains approximately 1200 g of calcium and has a daily intake of 1100 mg/day. There are no pubHshed exposure limits (38). Low levels of calcium in the blood, hypocalcemia, can lead to tetany high levels, hypercalcemia, can lead to coma and death. Calcium toxicity, above 160 mg/L in the blood, is not related to an excessive intake of calcium. 

Persistent activation of PPARa can induce the development of hepatocellular carcinoma in susceptible rodent species by a nongenotoxic mechanism, i.e., one that does not involve direct DNA damage by peroxisome proliferator chemicals or their metabolites. This hepatocarcinogenic response is abolished in mice deficient in PPARa, underscoring the central role of PPARa, as opposed to that of two other mammalian PPAR forms (PPARy and PPAR5), in peroxisome proliferator chemical-induced hepatocarcinogenesis. Other toxic responses, such as kidney and testicular toxicities caused by exposure to certain phthalate... 

Models based on Eqs. (47)-(50) have been used in the past to describe the disruption of unicellular micro-organisms and mammalian (hybridoma) cells [62]. The extent of cell disruption was measured in terms of loss of cell viability and was found to be dependent on both the level of stress (deformation) and the time of exposure (Fig. 25). All of the experiments were carried out in a cone and plate viscometer under laminar flow conditions by adding dextran to the solution. A critical condition for the rupture of the walls was defined in terms of shear deformation given by Eq. (44). Using micromanipulation techniques data were provided for the critical forces necessary to burst the cells (see Fig. 4)... 

Lucke-Huhle C, Pech M, Herrlich P. 1986. Selective gene amplification in mammalian cells after exposure to 60Co J rays 241Am a particles, or UV light. Radiat Res 106 345-355. 

This approach is not restricted to bacterial or viral cells. Mammalian cells under highly proliferating conditions can be cultured at increasing exposure to a compound in attempts to create resistant mutants. Alternatively, one can sometimes use a structural biology approach to predict amino acid changes that would abrogate inhibitor affinity from study of enzyme-inhibitor complex crystal structures. If the recombinant mutant enzyme displays the diminished inhibitor potency expected, one can then devise ways of expressing the mutant enzyme in a cell type of interest and look to see if the cellular phenotype is likewise abolished by the mutation. 

Due to the low volatility of cyromazine and the use of water-soluble bags for packaging the Trigard formulation, the main routes of exposure were expected to be from direct contact with the product or spray mixture on contaminated surfaces. Previous experience with pesticides worker exposure studies indicated that exposure from vapors or spray mist would be a minor factor. This can easily be confirmed by the PHED or similar published sources however, the extent of exposure from inhaling the product as dust is less well known. This route of exposure was also assumed to be minor, particularly with the use of water-soluble bag packaging. Given the low mammalian toxicity of cyromazine, the operators did not wear respiratory protection. 

Geller AM Health Effects Research Laboratory, Research, Triangle Park, NC The mechanisms, location, and severity of the effects of lead exposure on the mammalian retina National Institute of Environmental Health Sciences... 

No mortality was found in any embryo exposed to the controls. On the contrary, all the embryos exposed to the non-diluted samples of penta-, octa-, and deca-BDE commercial mixtures were dead after 24 h (Fig. 10). When the untreated PBDEs samples were diluted at 50%, a gradient of toxicity was observed penta > octa > deca. After dilution at 5%, no embryos exposed to untreated samples were dead. In agreement with our results, it has been demonstrated that the toxicity of deca-BDE is commonly lower than for octa- and penta-BDE commercial products exposures with mammalian models [64]. The different toxicity found in mammalian models and also in zebrafish should be related to the higher accumulation of lower brominated congeners in the body, because of their greater partitioning and retention in lipid-rich tissues and lower rates of metabolism and elimination in relation to deca-BDE. 

To develop a better understanding of the potential health consequences of radiocerium in our environment, it is important to know the possible sources and physical and chemical forms of its release. The metabolism and dosimetry of internally-deposited radiocerium are highly dependent upon the forms of the material presented to the body and the mode of exposure as discussed in Section 3—Metabolism of Cerium in Mammalian Species. 

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