The Effect Of Calcium Tainted Water On Cadmium Induced Liver Damage

Project and Seminar Material for Biochemistry

The Effect Of Calcium Tainted Water On Cadmium Induced Liver Damage


Abstract


The effect of calcium tainted water on cadmium induced liver damage has not been explored in our environment. 48 wistar rats were used for this study. The animals were randomly divided into eight (8) groups of five (5) rats each. Group A was the positive control and received 5 mg/kg body weight (bw) of cadmium chloride (CdCl2) intraperitoneally as a single dose. Groups B and C received the aqueous extract of zest of citrus sinensis (AEZCS) at a low doses of 10 and 40 mg/kg bw respectively. Groups D and E received cadmium chloride, followed by low and high doses of AEZCS respectively. Groups F and G received low and high doses of AEZCS followed by CdCl2 while group H served as the normal control. Liver enzymes (AST, ALT and ALP) and serum total proteins were analyzed. The results showed significant (P<0.05) differences in the mean values of LV/BW, ALT, AST, total proteins, serum dismutase (SOD) and malondialdehyde (MDA) when the positive control group was compared with the normal control group (P<0.05). Histological sections of the negative control groups were significantly different from the positive control group but not from the groups treated with AEZCS at the high doses. Thus, AEZCS had ameliorative and protective health benefits at the high dose of 40mg/kg body weight.


Chapter One


1.0 Introduction

1.1 Background Of The Study

Heavy metals are toxic agent. They are toxic to humans and animals. Heavy metals which establishes toxic actions to humans include; cadmium (Stohs and Bagchi,1995), lead ( Ferner, 2001) and mercury (Hawkes, 1997). Each of these has been studied in isolation for toxicity (Hutton and Symon, 1986; Nriagu and Pacyna, 1988; Nriagu, 1989). But, in the ecosystem, be it air, atmosphere, land, and water where they occur, they do not exist in isolation. They occur in close association with other metal and non-metallic elemental pollutants. Among the metallic pollutant could be calcium, copper, zinc, magnesium, manganese, iron and others. Metals are known to interact with one another. The interaction can bring two elements together in close proximity or it could cause out right displacement of one another. When ingested together in food and water, they antagonize each other. When it comes to intestinal and pulmonary absorption, it is therefore conceivable that the presence of other elements can the toxic potential of each of the heavy metals that have been studied in isolation.

Eborge (1994) reported that warri river has an unacceptable high cadmium level, 0.3 mg cadmium per liter of water which was 60 folds above the maximum allowable level of 0.005 mg per liter. This report prompted our earlier studies on the hepato, nephro and gonadial toxicity of cadmium. In rats exposed to this high dose via water and diet, the diet was formulated with feed exposed to 0.3 mg cadmium per water. In the ambient water as protein source and the toxic effect investigated and reported (Asagba and obi 2000; Asagba and Obi 2001; Obi and Ilori 2002; Asagba and Obi 2004a; Asagba and Obi 2004b; Asagba and Obi 2005).The study focus on cadmium without taking into consideration the fact that other metals were also present in the river water, and as such were co-consumed by the communities using the river water for cooking drinking and for other domestic purposes. Hence, it is desirable to know if the presence of other metals would enhance or diminish the toxic potential of cadmium or indeed if any other heavy metals such as lead that was mentioned above. Therefore, the aim of the present study was to re-examine the toxic potential of cadmium in the presence of other metals such as calcium and magnesium.


1.2 Statement Of Problem

Cadmium (Cd) is an important industrial and environmental toxicant with many industrial applications. Cd emissions to the atmospheric, aquatic, and terrestrial environment have increased during the last century. Since Cd is not degraded in the environment, the risk of human exposure is constantly increased due to Cd also enters to the food chain [1]. Humans are generally exposed to Cd by two main routes, inhalation and ingestion. Absorption of Cd by skin is relatively insignificant [2]. In humans and other mammals, Cd exposure can result in a variety of adverse effects, such as testicular damage, pulmonary edema, renal and hepatic dysfunction, osteomalacia, etc. In addition to the direct cytotoxic effects that could lead to apoptotic or necrotic event, Cd has been implicated in the development of cancer and it has been classified as a type I carcinogen by the International Agency for Cancer Research [3]. Emerging evidence suggests that Cd exposure affects Cytochrome P 450 1A1 (Cyp1A1). Cyp1A1 has been always associated with the transformation of pro-carcinogenic compounds to highly carcinogenic metabolites [4]. Chronic Cd intoxication results mainly in renal disease [5,6] but acute Cd exposure primarily results in liver accumulation and hepatocellular damage. After acute exposure to inorganic forms of Cd, the preponderance of the dose accumulates in the liver [7]. Cadmium retention is generally higher in women rather than men [8]. Gender differences in susceptibility, at lower exposure, are uncertain, but some data indicate that Cd has estrogenic effects and affects female offspring [8]. Humans are susceptible to Cd toxicity primarily through the ingestion of contaminated food or water and the inhalation of cigarette smoke. Today, nanotechnology with the development of Cd-containing nanoparticules, could be also a source of metal exposure [9]. Gastrointestinal ingestion of Cd through food or drinking water is the major route of intake for this metal in nonsmoking and non-occupationally exposed populations [10]. Cigarette smoke is the largest source of Cd exposure in general population. Each cigarette could contain up to 6.67 µg Cd, and 40-60% of it generally passes through the pulmonary epithelium into systemic circulation.


1.3 Objectives Of The Study

The objectives set out to achieve were;

  1. Re-examination of toxicity of using established and those for liver toxicity namely; blood alanine amino transferase and aspartate amino transferase, alkaline phosphatase, bilirubin, albumin and total protein.
  2. Re-examine the status parameter in the absence of cadmium but in the presence of calcium or magnesium or both.
  3. Re-examine this parameters in the presence of cadmium, calcium and magnesium.

Chapter Five


5.0 Summary And Conclusion

5.1 Summary

The effect of the AEZCS on the liver enzymes and total protein concentration showed that the liver injury induced through cadmium chloride administration culminated in increased concentrations of Alanine aminotransferease (ALT), Aspartate aminotransferease (AST) and alkaline amino phosphatase (ALP). The rise in levels of these enzymes particularly ALT, is in concordance with report in hepatocellular membrane damage. AEZCS administration at both lower and higher doses protected and maintained the liver function by moderating the activities of serum liver enzymes. Although this potency was more efficient at the high dose AEZCS at our higher dose, significantly lowered the serum liver enzymes activities which is increasingly altered in oxidative stress conditions. Though, this may not be a strong prognostic sign in fulminant liver injury, where there are major losses of functional hepatocyte. In the positive control group of rats, cadmium exposure significantly decreased the level of serum total proteins. The abnormal decrease has been associated to damage in the hepatic sinusoids and blood vessels in oxidative stress condition. A consequence of decrease in serum albumin being the major plasma protein is a shift of blood from the intravascular to interstitial spaces and peritoneal cavity resulting in intravascular volume depletion and edema formation (Busher, 1990). However, in the groups of pretreated and post treated with low and high doses of AEZCS before and after exposure to cadmium, there was a noticeable increment in the total protein suggesting its protective and ameliorative potency against cadmium induced serum protein depletion


5.2 Conclusion

Hepatotoxicity from most environmental toxicants has posed a predominant health risk in various populations especially in sub-Saharan Africa. The treatment options are few, usually expensive, less accessible and not synthetic treatment products since the extract of zest of C. sinensis contains important phytochemical constituents. From the results obtained in the research, the extract of the zest of citrus sinensis significantly protected and ameliorated liver associated with cadmium in our study environment. Hence, this research recommends that attempt should be made to insert the extract as residues in dietary supplements and in drug formulation for treatment of liver dysfunction associated with cadmium.


The Effect Of Calcium Tainted Water On Cadmium Induced Liver Damage


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The Effect Of Calcium Tainted Water On Cadmium Induced Liver Damage


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