Lead is a naturally occurring bluish-gray metal found in small amounts in the Earth’s crust and can be found in all parts of our environment (Gupta, 2007). Lead is found in our food, water, air and soil. Lead emitted by smelters and boilers that burn used motor oil is frequently deposited in the soil, where it is taken up by crops (Chiras, 2009). Lead is known as an enzymatic toxicant, is neurotoxic, hemato and cardiovascular toxic, nephrotoxic, immunotoxic, carcinogenic, teratogenic and mutagenic (Kiran et al., 2009; Moreira and Moreira, 2004). Lead damages cellular materials, alters cellular genetics and produces oxidative damage. It causes hyperproduction of free radicals and decreased availability of anti oxidant reserves to respond to the resultant damage. It also interrupts enzyme activation and competitively inhibits trace mineral absorption. Lead binds to sulfhydryl proteins (interrupting structural protein synthesis), alters calcium homeostasis and lowers the levels of available sulfhydryl antioxidant reserves in the body (Lynpatrick, 2006). The toxicity of lead is closely related to age, sex, route of exposure level of intake, solubility, metal oxidation state, retention percentage, duration of exposure, frequency of intake, casr rate, mechanisms and efficiency of excretion. Lead has been associated with various forms of cancer, nephrotoxicity, central nervous system effects and cardiovascular diseases in humans (Pitot and Dragan, 1996).
Captopril (D-3-mercapto-2-methyl-propanoyl-L-proline) is an angiotension-converting enzyme (ACE) inhibitor. Besides, its role as a treatment for hypertension (Sultana et al., 2007), it is commonly used as a cardioprotective drug (Khattab et al., 2005). Like other ACE inhibitors, captopril inhibits the conversion of angiotensin I, a relatively inactive molecule, to angiotensin II which is the major mediator of vasoconstriction and volume expansion induced by the renin–angiotensin system. Captopril, an inhibitor of angiotensin converting enzyme (ACE), has also been postulated as a free radical scavenger because of its terminal sulfhydryl group (Bagchi et al., 1989; Andreoli, 1993). Some in vitro studies indicate that captopril functions as an antioxidant both by scavenging ROS and by increasing the activities of antioxidant enzymes such as superoxide dismutase and glutathione peroxidase (Westlin and Mullane, 1988; Kojsova et al., 2006). Captopril has been shown to decrease serum lipid peroxide concentrations in diabetic patients (Ha and Kim, 1992).
Material and methods
Lead had been a toxic problem for human beings from the earliest time. The ingested and absorbed lead stored primarily in soft tissues and bone, but the highest concentration of lead occurs within the bone, teeth, liver, lung, kidney, brain and spleen (Plumlee, 2004; Mudipalli, 2007). The present study resulted in insignificant differences in liver and spleen indices between control and experimental lead groups, that run in agreement with (Allouche et al., 2011). Histological investigations revealed that lead acetate exposure resulted in marked changes in the liver these findings agreed with (Jankeer and El-Nouri, 2009; Muselin et al., 2010; Suradkar et al., 2010) they stated that rat exposure to lead acetate caused hepatotoxicity characterized by engorgement of blood vessels along with sinusoidal hemorrhage, infiltration, dilatation of central veins and vacuolar degeneration of hepatocytes. In the present study, lead reached the liver via the portal vein that the liver is the first organ exposed to internally absorbed nutrients and other xenobiotics so lead accumulated in the liver tissue caused severe alterations characterized by congested and dilated portal veins and degeneration in hepatic cells with moderate ballooning, severe inflammation, apoptotic cells and mild fibrosis. Most orally ingested lead is excreted, but a portion is absorbed and is transferred to the blood where lead binds to hemoglobin in the erythrocytes so lead is carried through the circulatory system by erythrocytes, virtually all tissues in the body can become exposed to the toxic metal, particularly hematopoietic and immune system (Goering, 1993; Gidlow, 2004; Lawrence and McCabe, 1995). In the spleen, phagocytes (macrophages and polymorphonuclear cells) are responsible for slowing the propagation of an invading pathogen, while an antigen-specific adaptive immune response (antibody- or cell-mediated) is being established. Lead was reported to inhibit macrophage function (Kowolenko et al., l988; Mauel et al., 1989) possibly by overloading macrophages with cellular debris and inhibiting macrophage production of nitric oxide (Tian and Lawrence, 1995). In the context of adaptive humoral and cellular immune responses, lead increased both B-cell and T-cell in vitro proliferation (Lawrence, 1981a–c; Warner and Lawrence, 1986; Razani et al., 1999). In the present study, administration of lead resulted in severe changes in the spleen represented by severe lymphoid necrosis, moderate diffusion of white pulp into the red pulp, diminished lymphoid follicles and appearance of large macrophages might be due to the production of debris of dead cells.