Int. J. Environ. Res. Public Health 2012, 9 488 tubulin sulfhytryl groups and MAPs, two major stabilizers of MTs. Our findings showing As3+-elicited biochemical pathology of MTs are summarized in Table 1. Table 1. Summary for As3+-elicited MT Biochemical Pathology. Figure# 1 2 Stressor/antagonist As3+ 5 µM, 20 µM. As3+ 10 µM. System MTs in RFL6 cells. Spindle MTs and chromosomal patterns in RFL6 cells. Tubulin proteins and mRNA in RFL6 cells. -tubulin protein and mRNA in the lung of rats. MT biochemical pathology by As3+ Disassembly of MTs. Spindle MT deficiency, cell division aberration, chromosome clustering, scattering and lagging. Increasing free tubulin pool, decreasing polymer tubulins, inhibiting I tubulin mRNA. Inhibition of lung β-tubulin protein and mRNA levels. 3 4 5 6 7 8 9 10 As3+ 5 µM, 10 µM, 20 µM. As3+ intratracheal instillation (2.02 mg As/kg body in the form of NaAsO2 in 100 μL physiological saline) once a week for 5 weeks. As3+ 20 µM, 40 µM, DTT 1 mM. As3+ 40 µM, DTT 1 mM. As3+ 10 µM, 20 µM, 40 µM, [3H]NEM (2 µCi/mL). As3+ 5 µM, 10 µM, 20 µM. As3+ 20 µM, NEM 25 µM, taxol 20 µM. As3+ 10 µM, nocodazole 5 µg/mL. Bovine brain tubulin polymerization in vitro. Bovine brain tubulin polymerization in vitro. NEM binding to pure tubulins free of MAPs in vitro. Metallothionein and - GCS proteins in RFL6 cells. MTs in RFL6 cells. Tubulins and MAPs in RFL6 cells. Inhibition of MT polymerization in vitro and DTT abolishing As3+ effects assessed by turbidimetry. Inhibition of MT polymerization in vitro and DTT abolishing As3+ effects conformed by EM. Blocking NEM binding to tubulins. Enhancement of -GCS and metallothionein expression. Taxol antagonized As3+ and NEM-induced MT disassembly. Suppression of tubulin and MAP expression, nocodazole as a positive control. Arsenic is a metalloid element existing in inorganic and organic forms and in different oxidative states (−3, 0, +3 and +5) which distribute in water, soil and air from nature and anthropogenic sources. High-level exposure to arsenic is involved in workers in metal smelting, wood preservation and semiconductor industries [1]. The acute inhalation of arsenic dust or fume resulted in gastrointestinal effects, and central and peripheral nervous disorders such as vomiting, diarrhea, bloody urine, anuria, shock, convulsion coma and death [1,30]. Chronic exposure to arsenic in humans, by inhalation and oral routes via contaminated water, food and air, are strongly associated with anemia, peripheral neuropathy, lesions and carcinogenesis in the lung, liver, bladder, skin, kidney, etc. [1]. As3+ is 60-times more toxic than As5+ [31]. As3+ has a high affinity for sulfhydryl groups in proteins, such as enzymes, receptors or coenzymes. Binding of As3+ to critical thiol groups of proteins may be important