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By Zaher A. Radi

The first thorough evaluate of cyclooxygenase inhibitors, together with their toxicity mechanisms and toxicopathological risks

Cyclooxygenases (COXs) are enzymes accountable for the formation of an enormous classification of organic mediators known as prostanoids. Prostanoids similar to prostaglandins mediate inflammatory and anaphylactic reactions. For these struggling with irritation and ache, the pharmacological inhibition of COXs, with non-steroidal anti inflammatory medications (NSAIDs), akin to ibuprofen, provides aid. but using NSAIDs can set off toxicological results to boot, resulting in capability health and wellbeing risks.

Comparative Pathophysiology and Toxicology of Cyclooxygenases offers a finished assessment of ways COX inhibitors have an effect on a number of physically platforms, particularly the toxicity mechanisms caused whilst the COX enzyme is inhibited. The ebook presents an advent to the invention of cyclooxygenases, their use as healing brokers, in addition to an ancient viewpoint. laying off gentle at the alterations in expression, pathophysiology, and toxicology of COX inhibitors throughout species, the booklet deals a scientific exam of the consequences and pathophysiology of COX inhibitors and their mechanisms of toxicity, starting with the GI tract. next chapters cover:

  • The pathophysiology of COX inhibition on bone, tendon, and ligament healing
  • COX inhibitors and renal procedure pathophysiology and mechanisms of toxicity
  • The pathophysiologic position of COX inhibition within the ocular system
  • COX inhibition and the respiration and cardiovascular systems

The booklet additionally sheds mild at the most modern study dedicated to constructing COX inhibitors with out antagonistic side-effects. the 1st e-book to provide a radical comparative examine the toxicological results of COX inhibitors in the course of the physique, this precious source might help develop the study and improvement of more secure and more beneficial COX drugs.

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Additionally, indometacin produced focal ulcers in the cecum. , 2003). A 4-week toxicity study of indomethacin was conducted in nonhuman primates (marmoset) in which indomethacin was administered by oral route at dose levels of 2, 6, and 12 mg/kg per day. All animals given the daily 12-mg/kg dose and one animal given 6 mg/kg per day died during the dosing period and within 20 days. , 1990). 26 CHAPTER 1 GASTROINTESTINAL TRACT Diclofenac (Cataflam, Voltarin) has a rapid absorption, a short-half life of approximately 2 h, and is metabolized in the liver by CYP2C in humans.

1973). , 2002). , 1995). , 2002). COX-1 inhibition alone does not cause GI injury. , 2002a). , 2009). , 2002). The effects of SC-560, rofecoxib, and indomethacin on the healing of colon lesions induced by dextran sulfate sodium (DSS) in the rat were investigated. , 2006). Okayama et al. (2001) found that SC-560 significantly worsened the severity of colonic damage in DSS-induced colitis in rats. , 2005). In healthy rats, neither the sNSAID rofecoxib nor the COX-1 inhibitor SC-560 when given alone at 20 mg/kg induced gastric mucosal injury.

Radi and N. K. Khan, Effects of cyclooxygenase inhibition on the gastrointestinal tract, Experimental and Toxicologic Pathology, 58, pp. 163–173. ) does of 10 or 20 mg/kg per day and GI effects were evaluated. Gastroduodenal ulcers and lesions occurred with indomethacin treatment at both doses. Additionally, indometacin produced focal ulcers in the cecum. , 2003). A 4-week toxicity study of indomethacin was conducted in nonhuman primates (marmoset) in which indomethacin was administered by oral route at dose levels of 2, 6, and 12 mg/kg per day.

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