Handbook of Vitamin C Research

Protective Effect of Vitamin C 331Elemental mercury can be found in commonly-used objects such as glass thermometers,electric switches, fluorescent light bulbs and some medical equipment. Another use ofmercury is as dental composite fillings in primary molars, but it has recently been replaced inmost developed countries by bismuth, which has properties similar to mercury but shows lesstoxicity. Inorganic mercury can be found in batteries, chemistry laboratories, somedisinfectants and some types of drugs. The principal source of organic mercury exposure tohumans is fish, which is enriched in methylmercury. Dietary methylmercury is absorbed fromthe gastrointestinal tract, readily enters the bloodstream and is distributed to all tissues inabout 30 hours. Methylmercury is accumulated in hair and toenails, which both can be usedas indicators of long-term mercury exposure in population studies.1.1. Molecular Mechanism of Mercury ToxicityExposure to toxic levels of inorganic mercury mainly results in neurologic and renaldamage. Organic mercury compounds show less ability to produce nephrotoxicity. As withother heavy metal exposure, mercury toxicity has been mainly attributed to oxidative stressprocesses (Figure 1).Figure 1. Mechanisms implicated in mercury intoxication.In the kidney, the pars recta of the proximal tubules of the nephrons are the mostsusceptible regions for the toxic effects of mercury [3]. This nephrotoxicity related tomercury compounds is due to the binding capacity of mercury to proteins and to moleculesinvolved in the transport and uptake of ions into renal tubular cells [4]. Mercury has a highaffinity to bind to reduced sulphur atoms, especially to thiol-containing molecules such asglutathione, cysteine, homocysteine, N-acetylcysteine and albumin [5]. Plasma mercury bindsto albumin and other large plasma proteins.There are several studies suggesting that mercury exposure induces oxidative stress.Oxidative stress-induced by mercury seems to be mainly mediated by thiols depletion,especially gluthatione. Lund et al. demonstrated that low doses of mercury may avoidmitochondrial glutathione, enhancing hydrogen peroxide formation [6]. Increased levels ofhydrogen peroxide increases the oxidative processes favouring lipid peroxidation. Lipidperoxidation processes induced by mercury exposure seems to affect a number of organs. In