Gastrointestinal tract radicals

Primaquine is readily absorbed from the gastrointestinal tract, and in contrast to chloroquine, it is not bound extensively by tissues. It is rapidly metabolized, and the metabolites are reported to be as active as the parent drug itself. Peak plasma levels are reached in 4 to 6 hours after an oral dose, with almost total drug elimination occurring by 24 hours. The half-life is short, and daily administration is usually required for radical cure and prevention of relapses. 

In addition, flavonoids have been found to be free-radical scavengers, and free radicals play an important role in ulcerative and erosive lesions of the gastrointestinal tract. In relation to their... 

The comparison of iron(II) and iron(III) uptake by mammalian intestine has recently been the focus of intense research effort. In a study of 14 different iron preparations in man, Dietzfelbinger [100] showed that the iron(III) preparations, without exception, had a lower bioavailability than iron(II) sulphate and were therefore of dubious therapeutic efficacy. Unfortunately, orally administered iron(II) sulphate generates hydroxyl radicals in the gastrointestinal tract of mammals [101], This property, together with the associated acidity of iron(II) sulphate, may cause irritation and damage to the mucosa. A wide range of side effects have been reported for iron(II) sulphate [102]. Thus, should an efficiently absorbed iron(III) complex be identified, it would be of therapeutic benefit. 

The gastrointestinal tract is also susceptible. DA vapor in partieular produces a phenyl radical that causes vomiting. Vomiting usually develops within 1-2 min after exposure to DA. 

Aspirin can also play a role in esophageal bleeding, ulceration, or benign stricture, and it should be considered as a possible cause in patients, particularly the elderly, who present with any of these features. There have also been reports of rectal stricture in the elderly, associated with the use of aspirin suppositories. Effects on both these strictures emphasize the significance of a direct local action of aspirin as well as a systemic action and underlines the relevance of the involvement of oxygen-derived free radicals in the pathogenesis of mucosal lesions in the gastrointestinal tract (54-56). 

CCI3 radical can yield trichloromethanol, a precursor to carbonyl chloride (phosgene). Since reactive metabolites are responsible for the bulk of the toxicity, tissues rich in CYP2E1, such as the liver and kidney, are the most sensitive toxicity targets for the compound. The unmetabolized fraction also produces some toxicity, and is associated with central nervous system (CNS) depression and irritation of the gastrointestinal tract. 

Halliwell, B., Zhao, K., and Whiteman, M., The gastrointestinal tract a major site of antioxidant action Free Radical Res., 33, 819-830, 2000. 

Another line of investigation is bridging polyphenol activity with NO bioavailability via the chemical reduction of nitrite to NO (Takahama et al, 2002 Peri et al, 2005 Gago et al, 2007). The redox properties that have been proposed to confer polyphenols with antioxidant activity by quenching oxidizing radicals may, alternately, endow the phenolic compounds with the capacity to promote the formation of NO from nitrite, particularly in the gastrointestinal tract, a location where both nitrite and polyphenols achieve high concentrations. 

Halliwell, B., K. Zhao, and M. Whiteman. 2000. The gastrointestinal tract A major site of antioxidant action Free Radic. Res. 33 819-830. 

During its many years of use as a consumer product, carbon tetrachloride compiled a grim record of toxic effects that led the U.S. Food and Drug Administration (FDA) to prohibit its household use in 1970. It is a systemic poison that affects the nervous system when inhaled, and the gastrointestinal tract, liver, and kidneys when ingested. The biochemical mechanism of carbon tetrachloride toxicity involves reactive radical species, including... 

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