(2001) with arsenite-exposed human lung A549, kidney UOK123, UOK109 and UOK121 cells isolated eight different DNA fragments by methylation-sensitive arbitrarily primed polymerase chain reactions. It turned out that six of the fragments were hyper- and two of them were hypomethylated. Higher levels of DNA methyltransferase mRNA and enzyme activity were found.Kitchin (2001) proposed a model of altered growth factors which lead to cell proliferation and thus to carcinogenesis. From observations, it is known that chronic low-dose arsenic poisoning can lead to increased tolerance to its acute toxicity. MRP1-overexpressing lung tumor GLC4/Sb30 cells poorly accumulate arsenite and arsenate. This is mediated through MRP-1 dependent efflux. The efflux requires glutathione, but no arsenic-glutathione complex formation.Although many mechanisms have been proposed, no definite model can be given for the mechanisms of chronic arsenic poisoning. The prevailing events of toxicity and carcinogenicity might be quite tissue-specific. Current consensus on the mode of carcinogenesis is that it acts primarily as a tumor promoter. Its co-carcinogenicity has been demonstrated in several models. However, the finding of several studies that chronically arsenic-exposed Andean populations (as most extremely exposed to UV-light) do not develop skin cancer with chronic arsenic exposure, is puzzling. Causes
Organic arsenic is less harmful than inorganic arsenic. Seafood is a common source of the less toxic organic arsenic in the form of arsenobetaine. The arsenic reported in 2012 in fruit juice and rice by Consumer Reports was primarily inorganic arsenic.
Nonocular (not eye-related) side and adverse effects can include neuropsychiatric symptoms like subtle concentration and memory problems, subtle decision-making problems, drowsiness, and more pronounced disorientation to time and place, confusion, disturbances of speech and movement, hyperactivity, restlessness, and seizures. Temporary psychosis can develop that includes hallucinations, particularly when higher doses are used in children or older adults on other anticholinergic medications. Patients with dementia of the Alzheimers type can experience worsening of their dementia symptoms. Additional side and adverse effects can include skin flushing, skin rashes, gastrointestinal problems, increased heart beat (tachycardia), increased body temperature (hyperpyrexia), blood vessel dilation, urinary retention, dry mouth and reduced sweating, and reduced bronchial secretions. Severe poisoning with cyclopentolate may result in coma, paralysis of breathing, and death. Cyclopentolate derivatives can be used as an antidote for organophosphate poisoning.Lethality of cyclopentolate has been studied in rodents. The LD50 (the dose at which 50% of animals die from the drug) is approximately 4000 mg/kg in rats and 960 mg/kg in mice. Readily recognizable symptoms of overdose include tachycardia, dizziness, dry mouth, behavioral disturbances, uncoordination, and drowsiness. Cycloplegia is necessary in cases of suspected latent hyperopia (or "over-focusing") so that an ophthalmologist or optometrist can accurately measure how much a person has to flex their focusing muscle (accommodation) in order to see in the distance and up-close. Correction of latent hyperopia in children can often prevent, or sometimes correct, unwanted eye turns (strabismus), some forms of refractive amblyopia, and may alleviate eye strain or frontal headaches caused by prolonged near-work.