Toxicants affecting

Selenium is an essential element and is beneficial at low concentrations, serving as an antioxidant. Lack of selenium affects thyroid function, and selenium deficiencies have been linked to Keshan Disease (34). Selenium at high levels, however, is toxic. Hydrogen selenide (which is used in semiconductor manufacturing) is extremely toxic, affecting the mucous membranes and respiratory system. However, the toxicity of most organ oselenium compounds used as donor compounds for organic semiconductors is not weU studied. 

There is only a limited capacity to metabolize vitamin A, and excessive intakes lead to accumulation beyond the capacity of binding proteins, so that unbound vitamin A causes tissue damage. Symptoms of toxicity affect the central nervous system (headache, nausea. 

All insecticides affected the mobility of . riparius larvae in a similar manner. A normal swimming motion was generally reduced to 1 cycle at the onset of toxic symptoms. The effect of the toxicant increased until the larva lost all ability to move. Death soon followed. Similar symptoms of insecticide poisoning have been reported for stonefly naiads (13, 14). Changes in larval color were unreliable for determining toxic affect. Toxic symptoms were observed in approximately 50-75% of the midge larvae immersed in 20 ug/L aldrin at the end of the 2 hr exposure but no effects were noted with aldrin plus PBO. All larvae immersed in dieldrin, or dieldrin with PBO were moribund. 

As previously described for the male reproductive toxicity, the class of toxicants affecting germ cells can alter the structure of genetic material (chromosomal aberrations, alterations in meiosis, DNA synthesis, and replication). Mature oocytes have a DNA repair capacity different from that of mature sperm, but this capacity decreases at the period of meiotic maturation. 

Toxicants can affect any type of tissue in any organ. Different classes of toxicants affect various tissues to varying degrees and in a variety of ways, depending on the nature of the toxicant, the kind of receptor that it attacks, the nature of the binding of the toxicant to the receptor, and the routes, transport, and metabolism of the toxicant in the organism. 

What are the chronic toxicological effects of benzene What kinds of blood abnormalities are caused by benzene exposure How does benzene toxicity affect white cell count How does it affect bone marrow ... 

Kidney Drug toxicity affecting kidney Rat model MALDI-MSI NMR-HRMAS LC-MS Identification and mapping of renal crystalline deposits Identification of molecular changes in pathological areas (59)... 

Toxic affects of 2-fluoro-L-histidine (2-FHis) (98) on bacteria have been attributed in part to the action of this analogue as a potent feed back inhibitor of ATPiphosphoribo-syl transferase, the first committed enzyme in histidine biosynthesis. No other halogenated analogues of histidine were active in this regard155. 

Benzene, however, is quite different in that it s toxicity affects the blood forming organs. 

Specific toxicity (affects only sensitive crops)... 

The chronic toxicity of vitamin A is a more general cause for concern prolonged and regular intake of more than about 7,500 to 9,000 /rg per day by adults (and significandy less for children) causes signs and symptoms of toxicity affecting ... 

Care should be exercised when toxicants affecting more than one organ system are combined that the potentiation or synergistic interactions are considered, because certain substances can cause target organ toxicity at <1% concentration when other ingredients in the mixture are known to potentiate its toxic effect. 

TNM is highly toxic affecting respiratory organs and the nervous system. According to the American Industrial Hygiene Association (197) the permitted concentration in air is 0,001 ing/l, A considerable number of papers have been published on the toxicity and pharmacology of TNM (198-2031. 

Most drugs are proved to be safe through a series of short- (acute) and long-term (chronic) tests. No drugs that show adverse toxic affects when tested as singledose study will make it into the long-term study programs. 

The basic assumptions made in order to model the impacts of toxicants on the competitive interactions discussed above are (1) the toxicant affects the metabolic pathways used in the consumption of a resource and (2) this alteration of the metabolism affects the growth rate vs. resource curve. In terms of resource competition, the consumption vector is changed, and the shape and placement of the ZNGI is altered. In the following discussions the implications of these changes on examples using essential resources are depicted. 

Predation. Often a toxicant affects more than one species. Perhaps the predators, disease organisms, or herbivores that crop a food resource are affected by the toxicant. Predation is an important aspect of mortality. 

An inhibiting chemical slows the enzymatic metabolism of a toxic chemical. In this instance, if the uptaken chemical itself is the toxin, inhibition will slow the metabolism and intensify its action. If the metabolite of the absorbed xenobiotic is the toxic agent, inhibition will decrease the toxic affect. Vinyl chloride uptake in rats results in the lowering of cytochrome P450 and a corresponding loss of ability to metabolize other xenobiotics. Other inhibitors include diethyl maleate, which inhibits glutathione s-transferase and 1-aminobenzotriazole, which inhibits P450. 

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