The effects of some boron compounds against heavy metal toxicity in human blood

Abstract

Heavy metals can accumulate in the environment and cause serious damages to ecosystems and human health. Boron is considered to be essential micronutrient with its well established biological functions and the antioxidant effects of boric acid (BA) are controversial. However, the potential of important boron compounds in cellular activities remains unexplored. Therefore, we aimed to assess the efficacies of some boron compounds (BA, borax, colemanite and ulexite) on the genotoxicity induced by heavy metals (arsenic trioxide, colloidal bismuth subcitrate, cadmium chloride, mercury chloride and lead chloride) in human blood cultures. For this aim, sister chromatid exchange (SCE) and micronuclei (MN) assays were performed to establish DNA damages in lymphocytes. Besides, oxidative stress was monitored by estimating the changes of main antioxidant enzyme activities and the levels of total glutathione (TGSH) in erythrocytes. The present study showed that heavy metal treatments increased the frequencies of SCE and MN and the plasma malondialdehyde (MDA) level; decreased the antioxidant enzyme activities and the level of TGSH compared to controls. Whereas, the tested boron compounds (5–20 ppm) significantly reduced the genotoxic effects induced by low doses of heavy metals. Our results revealed that the protective roles of boron compounds occurred with the effectiveness on their anti-oxidant capacity. In conclusion, these compounds could be useful in the development of functional food and raw materials of medicine.

Introduction

Arsenic (As), cadmium (Cd), mercury (Hg) and lead (Pb) are common environmental pollutants. These metals have no beneficial effects in humans, and there is no known homeostasis mechanism for them (Llobet et al., 2003). Among industrially used and mined heavy metals, bismuth (Bi) is one of the least toxic of the heavy metals. However, intoxication with Bi has occurred from its use in medicine (Lewis, 1996). The general population is exposed to heavy metals at several concentrations either voluntarily through supplementation or involuntarily through intake of contaminated food and water or contact with contaminated soil, dust, or air (Meeker et al., 2008). And exposure to these toxic metals is associated with many serious diseases including Alzheimer's (Mutter et al., 2007), Parkinson's (Guzeva et al., 2008), autoimmune (Ohsawa, 2009), digestive (Borges et al., 2008), heart (Saad et al., 2006) disorders and liver, kidney, stomach and lung cancers (Waalkes, 2000, Vahter, 2007). One of the major mechanisms behind metal toxicity has been attributed to oxidative stress (Flora et al., 2008). In fact, various studies connect heavy metals with oxidative DNA damage, since these metals may reduce the level of the main antioxidant compounds in several animal tissues by inactivating enzymes and other antioxidant molecules (Chater et al., 2008, Jihen et al., 2009).

On the other hand, boron, the fifth element in the periodic table, is a naturally occurring element. In the environment, boron is combined with oxygen and other elements in compounds called borates. Borates are widely found in nature, and are present in oceans, rocks and soils. There are several commercially important borates, including BA, borax (BX) and the minerals colemanite (COL) and ulexite (UX) (Cotton and Wilkinson, 1998). These compounds are widely used in industrial, agricultural, cosmetic, medical settings, household products and a numerous smaller applications (Fail et al., 1998, Pahl et al., 2005). The boron, a trace mineral for plants, animals and humans, has been shown to have apparent beneficial effects in humans at intakes commonly found in diets abundant in foods such as fruits and vegetables (Nielsen, 1996, Devirian and Volpe, 2003). Research findings suggest that physiological amounts of supplemental dietary boron (as BA) affect a wide range of metabolic parameters in animals (Hunt, 1998). It probably strengthens the antioxidant defense mechanism by a yet unknown mechanism (Pawa and Ali, 2006). Orally administered boron is rapidly and completely absorbed from the gastrointestinal tract into the blood stream (Usuda et al., 1998) and plays an important role in improving arthritis, plasma lipid profiles, brain function (Devirian and Volpe, 2003). A variety of boronated agents with hypolipidemic, anti-inflammatory or anticancer properties is also developed (Barranco et al., 2008). Moreover, the boron compounds show minimal potential for genotoxicity in bacteria and cultured mammalian cells (Moore and Expert Scientific Committee, 1997, Turkez et al., 2007). Thus, these compounds remain very interesting research topics due to equivocal and relatively unknown useful actions, roles in the treatment of various diseases, and interactions of other elements.

Since the complete avoidance of exposure to heavy metals is very difficult, chemoprevention is a popular strategy for protecting humans and animals from the risk of serious health problems by exposure to these toxic metals. Several antioxidants including vitamins (Appenroth and Winnefeld, 1998, Fahmy et al., 2008), N-acetyl-cystein (Ustundag and Duydu, 2007), taurine (Bosgelmez et al., 2008), bioflavonoids (Ponnusamy et al., 2008) were tested for their effectiveness in minimizing heavy metals-induced oxidative DNA damages. However, to the best of our knowledge, the effects of boron compounds against metal toxicities were not yet studied. Therefore, the present study was conducted to evaluate the efficacy of four main boron compounds; BA, BX, COL and UX in genotoxicity induced by arsenic trioxide (As₂O₃), cadmium chloride (CdCl₂), lead chloride (PbCl₂), colloidal bismuth subcitrate (C₆H₅O₇Bi) and mercury chloride (HgCl₂) exposures in peripheral human blood cultures. For this purpose, SCE and MN tests covering a wide range of induced genetic damage as primary DNA damage were performed on peripheral lymphocytes. Also, the oxidant-antioxidant status of blood cultures were assessed by measuring superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), TGSH and MDA.