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Reprotoxic and Endocrine Substances
Published in Małgorzata Pośniak, Emerging Chemical Risks in the Work Environment, 2020
Katarzyna Miranowicz-Dzierżawska
The following pharmaceuticals are known to impair the function of male reproductive organs: cytostatics – used in cancer therapy; lithium salts, which due to their effectiveness remain a common medication in the treatment of bipolar disorder; methyldopa – an antihypertensive medicine; and levodopa – used in the treatment of Parkinson’s disease. Moreover, impotence, ejaculation disorders, and decreased libido can occur after exposure to the following pharmaceuticals: spironolactone, clonidine, rilmenidine, guanethidine, prazosin, perhexiline, reserpine – antihypertensive medicine; cimetidine – a histamine receptor antagonist; as well as in therapies using corticosteroids, neuroleptics (thioridazine) and disopyramide, used for the treatment of arrhythmia. Sulfasalazine, used in the treatment of ulcerative colitis and Crohn’s disease, can also cause fertility disorders in males [Skowron et al. 2011]. Warfarin (a drug used to reduce blood clotting) or retinoids (used in dermatology) can also have a teratogenic effect.
Carbon Monoxide — From Tool to Neurotransmitter
Published in David G. Penney, Carbon Monoxide, 2019
Nanduri R. Prabhakar, Robert S. Fitzgerald
Molecular characterization revealed the existence of two distinct forms of heme oxygenase designated as HO-1 and HO-2 with differing characteristics (Kutty and Maines, 1989; Maines, 1988; Muller et al., 1987; Rotenberg and Maines, 1988). The most striking difference between the two forms is that HO-1, but not HO-2, can be induced by a variety of stimuli (Table 2). Metal ions like cobalt chloride were the first group of chemicals that were shown to induce HO-1 (Maines and Kappas, 1974). Other metals that affect HO-1 include aluminum, tin, mercury, lead, and gold. In addition to the metals, a host of exogenous and endogenous chemicals as well as diverse factors such as X-ray irradiation, stress, fever, starvation, etc. can induce HO-1 activity. Some of the endogenous and exogenous chemicals that induce HO-1 activity include heme compounds, cemetidine (an histamine receptor antagonist), epinephrine, insulin, bacterial antigens, glucocorticoids, etc. (Maines, 1988). Hypoxia is another potent inducer of HO-1 in endothelial cells (Jornot and Junod, 1993).
Flavonoids from Quercus Genus: Applications in Melasma and Psoriasis
Published in Tatjana Stevanovic, Chemistry of Lignocellulosics: Current Trends, 2018
Esquivel-García Roberto, Velázquez-Hernández María-Elena, Valentín-Escalera Josué, Valencia-Avilés Eréndira, Rodríguez-Orozco Alain-Raimundo, Martha-Estrella García-Pérez
An increase in the number of mast cells has been detected in pigmented lesional dermis of melasma patients but its role in melasma has not been completely examined. However, as in other dermatological diseases, histamine released by mast cells could rise melanin synthesis by binding to histamine receptor in melanocytes, particularly H2, through intracellular cAMP signaling pathway activation. Mast cells can also induce vascular proliferation by secreting angiogenic factors such as vascular endothelial growth factor (VEGF). There is an increase of this cytokine and in blood vessel of melasma lesion that produce altered dermal vasculature (Kim et al. 2007, Lee 2015, Kwon et al. 2016). Evidence of damage to basal membrane (BM), which could facilitate the migration of active melanocytes and melanin into the dermis has also been reported. This damage could be produced through an increase in the activity of mast cell tryptase and matrix metalloproteinases (MMP) that cause the degradation of collagen in the skin during chronic UV exposure (Torres-Álvarez et al. 2011).
World Trade Center Health Program best practices for the diagnosis and treatment of gastroesophageal reflux disease
Published in Archives of Environmental & Occupational Health, 2023
Ruth A. Lin, Geoffrey M. Calvert, Iris G. Udasin
PPIs suppress acid production by irreversibly blocking the H+K+-ATPase proton pump in gastric parietal cells. As a result, PPIs raise the pH of the gastric reflux into the esophagus. H2RAs compete for histamine receptors in the gastric parietal cells and block acid production. Decreased acidity limits the damage of the gastric reflux in the esophagus. Summaries of the mechanism of action and scientific basis of these medications are available.16,17