Phytoremediation of heavy metals—Concepts and applications

Even in the current era of growing technology, the concentration of heavy metals present in drinking water is still not within the recommended limits as set by the regulatory authorities in different countries of the world. Drinking water contaminated with heavy metals namely; arsenic, cadmium, nickel, mercury, chromium, zinc, and lead is becoming a major health concern for public and health care professionals. Occupational exposure to heavy metals is known to occur by the utilization of these metals in various industrial processes and/or contents including color pigments and alloys. However, the predominant source resulting in measurable human exposure to heavy metals is the consumption of contaminated drinking water and the resulting health issues may include cardiovascular disorders, neuronal damage, renal injuries, and risk of cancer and diabetes. The general mechanism involved in heavy metal-induced toxicity is recognized to be the production of reactive oxygen species resulting oxidative damage and health related adverse effects. Thus utilization of heavy metal-contaminated water is resulting in high morbidity and mortality rates all over the world. Thereby, feeling the need to raise the concerns about contribution of different heavy metals in various health related issues, this article has discussed the global contamination of drinking water with heavy metals to assess the health hazards associated with consumption of heavy metal-contaminated water. A relationship between exposure limits and ultimate responses produced as well as the major organs affected have been reviewed. Acute and chronic poisoning symptoms and mechanisms responsible for such toxicities have also been discussed.

Prevalence of exposure of heavy metals and their impact on health consequences

Nickel-induced toxicity and carcinogenicity, with an emphasis on the generation and role of reactive oxygen species is reviewed. Nickel is a known haematotoxic, immunotoxic, neurotoxic, genotoxic, reproductive toxic, pulmonary toxic, nephrotoxic , hepatotoxic and carcinogenic agent. This article presents a selective review on nickel and effect of its acute, subchronic and chronic doses on certain metabolically active tissues in human as well as animals. Nickel exposure causes formation of free radicals in various tissues in both human and animals which lead to various modifications to DNA bases, enhanced lipid peroxidation, and altered calcium and sulphydryl homeostasis. The primary route for nickel toxicity is depletion of glutathione and bonding to sulphydryl groups of proteins. Nickel homeostasis, nickel-induced activation of signaling pathways and the protective role of enzymatic and non-enzymatic antioxidants against nickel toxicity and carcinogenicity are also discussed.

Nickel, its adverse health effects & oxidative stress.

As technology continues to advance, heavy metals in drinking water have exceeded recommended limits from regulators around the world. The main source of human exposure to heavy metals is from contaminated drinking water. The effects of drinking water contaminated with heavy metals, such as arsenic, lead, nickel, cadmium and mercury, have gradually caught the attention of the relevant departments and personnel. It is well known that occupational exposure to heavy metals occurs as a result of using these metals in a variety of industrial processes in and/or a variety of materials, including color pigments and alloys. A series of adverse effects on human metabolism has resulted from exposure to heavy metal-contaminated drinking water, which has been recorded from around the world. The general mechanism of heavy metal toxicity is through the production of reactive oxygen species, the appearance of oxidative damage, and subsequent adverse effects on health. Therefore, water contaminated with heavy metals causes high morbidity and mortality worldwide. In order to address concern regarding the health effects of different heavy metals, this paper reviews its sources, distribution and effects of heavy metal on human metabolism.HIGHLIGHTSThe accumulation of heavy metals such as lead, arsenic, mercury, cadmium and nickel will destroy the main metabolic process of human body.Redox reactions in biological systems are caused by carcinogenic metal ions such as nickel and arsenic. The free radicals produced by these reactions cause oxidative damage to proteins and DNA.The accumulation of heavy metals eventually produces reactive oxygen species that can cause oxidative stress, which may lead to the production of various diseases.

The effects of heavy metals on human metabolism.

Environmental profiles for the selected metals were compiled on the basis of available data on their biological activities. Analysis of the profiles suggests that the concept of toxic heavy metals and safe nontoxic alternatives based on lighter metals should be re-evaluated. Comparison of the toxicological data indicates that palladium, platinum, and gold compounds, often considered heavy and toxic, may in fact be not so dangerous, whereas complexes of nickel and copper, typically assumed to be green and sustainable alternatives, may possess significant toxicities, which is also greatly affected by the solubility in water and biological fluids. It appears that the development of new catalysts and novel applications should not rely on the existing assumptions concerning toxicity/nontoxicity. Overall, the available experimental data seem insufficient for accurate evaluation of biological activity of these metals and its modulation by the ligands. Without dedicated experimental measurements for particular metal/ligand frameworks, toxicity should not be used as a "selling point" when describing new catalysts.

Which Metals are Green for Catalysis? Comparison of the Toxicities of Ni, Cu, Fe, Pd, Pt, Rh, and Au Salts.

Nickel exposure greatly depletes intracellular ascorbate and alters ascorbate-cholesterol metabolism. We studied the effect of the simultaneous oral treatment with L-ascorbic acid (50 mg/100 g body weight (BW) and nickel sulfate (2.0 mg/100 g BW, i.p) on nickelinduced changes in serum lipid profiles and liver histopathology. Nickel-treated rats showed a significant increase in serum low-density lipoprotein-cholesterol, total cholesterol, triglycerides, and a significant decrease in serum high-density lipoprotein-cholesterol. In the liver, nickel sulfate caused a loss of normal architecture, fatty changes, extensive vacuolization in hepatocytes, eccentric nuclei, and Kupffer cell hypertrophy. Simultaneous administration of L-ascorbic acid with nickel sulfate improved both the lipid profile and liver impairments when compared with rats receiving nickel sulfate only. The results indicate that L-ascorbic acid is beneficial in preventing nickel-induced lipid alterations and hepatocellular damage.

Effect of L-ascorbic acid on nickel-induced alterations in serum lipid profiles and liver histopathology in rats.

We have studied the effect of simultaneous oral treatment of aqueous garlic extract (Allium sativum) on heavy metal (nickel II and chromium VI) induced changes in serum lipid profile. Nickel sulfate and potassium dichromate treated rats showed a significant increase in serum low density lipoprotein-cholesterol (LDL-C), very low density lipoprotein-cholesterol (VLDL-C) and triglyceride (TG) level as well as decrease in serum high density lipoprotein-cholesterol (HDL-C) level. Simultaneous garlic administration with nickel sulfate showed improvement in serum LDL-C, HDL-C, VLDL-C and TG level. But in case of potassium dichromate, garlic administration did not show satisfactory improvement in lipid profile except VLDL-C and TG level. The results indicate that garlic (Allium sativum) has some beneficial effect in preventing heavy metal (nickel and chromium VI) induced alteration of lipid profile.

/pdf/effect-of-garlic-allium-sativum-on-heavy-metal-nickel-ii-and-1f3elmc901.pdf

Effect of Garlic (Allium sativum) on Heavy Metal (Nickel II and ChromiumVI) Induced Alteration of Serum Lipid Profile in Male Albino Rats

In this experimental study, we investigated whether L-ascorbic acid has any influence on the blood antioxidant defense system, lipid peroxidation and hematological parameters of the albino rats exposed to nickel sulfate(NiSO4). Twenty four adult rats were divided into four groups of six animals in each group. The control rats were untreated and comprised Group I. Group II rats were administered nickel sulfate (2.0 mg/100 g b.wt.; intraperitonially, i.p.). Group II rats were treated orally L-ascorbic acid (50 mg/100 g b.wt.) and Group IV rats were given both nickel sulfate and L-ascorbic acid simultaneously on alternate days until the tenth dose. The hematological parameters were assessed: red blood corpuscle counts, packed cell volume %, hemoglobin concentration, white blood corpuscle counts and platelets count decreased significantly and clotting time increased significantly in nickel treated rats. We also observed increase malondialdehyde (MDA) and decrease glutathione level (GSH) in erythrocytes of nickel treated rats. The activities of erythrocyte antioxidant enzymes like superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) were significantly increased in rats treated with nickel sulfate. Simultaneously treatment of L-ascorbic acid exhibited a possible protective role on the toxic effect of nickel sulfate on the hematological values, erythrocyte MDA and GSH concentrations as well as antioxidant enzymatic defense system.

Protective role of L-ascorbic acid on antioxidant defense system in erythrocytes of albino rats exposed to nickel sulfate.

We studied the effect of oral supplementation with L-ascorbic acid (50 mg /100 g body weight (BW) on nickel sulfate (2.0 mg/ 100 g BW, i.p)-induced lipid peroxidation and histopathology in the lung of Wister strain male albino rats. Lipid peroxide and glutathione levels and the activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), were estimated. Nickel sulfate administration significantly increased the level of lipid peroxides and decreased all antioxidant enzyme activities. Nickel sulfate treatment also induced (a) loss of normal characteristics and architectural organization, (b) inflammation in bronchioles, (c) alveolar congestion, (d) alveolar cell hyperplasia, and (e) congestion in the lumen. The simultaneous administration of L-ascorbic acid and nickel sulfate improved both lipid peroxidation and the histopathology of lung when compared with rats receiving nickel sulfate alone. The results indicate that L-ascorbic acid prevents nickel-induced alteration of antioxidant defense mechanisms and histopathology of lung tissue.

Salim A Dhundasi

Papers

Nickel, its adverse health effects & oxidative stress.

Effect of L-ascorbic acid on nickel-induced alterations in serum lipid profiles and liver histopathology in rats.

Effect of Garlic (Allium sativum) on Heavy Metal (Nickel II and ChromiumVI) Induced Alteration of Serum Lipid Profile in Male Albino Rats

Protective role of L-ascorbic acid on antioxidant defense system in erythrocytes of albino rats exposed to nickel sulfate.

L-ascorbic acid protects the antioxidant defense system in nickel-exposed albino rat lung tissue.