الفهرس 
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Abstract
Exposure to toxic substance can affect the body in many ways.in general, when chemicals and other toxic substances are absorbed, they travel through the various body systems and can affect a particular organs, called the target organs. the body has mechanisms, mainly in the liver and kidneys, to process and eliminate many of these substances.
Liver diseases:
Liver has important functions in the body, including
detoxification, plasma protein synthesis and glycogen storage (Yang et
al., 2011). Because of its unique metabolism and relationship to the
gastrointestinal tract, the liver is a crucial target of the toxicity of drugs,
xenobiotics and oxidative stress (Jaeschke et al., 2002). Liver is the
key organ of metabolism and excretion so it is continuously and
variedly exposed to xenobiotics because of its strategic placement in
the body (Shaker et al., 2010).
Evidences developed over the last several years have suggested
that various forms of liver injury may be caused by free radical
formation and subsequent oxidative stress (Bhadauria et al., 2008).
Also Loguercio and Federico (2003) stated that all processes that
involve hepatocyte, Kupffer, stellate and endothelial cells which induce
liver disease are related to the crucial role of reactive oxygen and
nitrogen species. It is believed that reactive oxygen species (ROSs),
such as hydroxyl radical, super oxide radical anion and nitric oxide
may injure cell membranes through lipid peroxidation and damage
biomolecules, i.e., proteins, lipids, carbohydrates and DNA in vitro and
in vivo (Halliwell, 1996 and Graziewicz et al., 2002). Documented
evidence has been reported that reactive oxygen species (ROSs),
including singlet oxygen, super oxide and hydroxyl radicals are knownto play an important role in liver-disease pathology and progression
(Vitaglione et al., 2004).
Significant cellular damage occurs when the amount of produced
free radicals exceeds the capacity of endogenous cellular antioxidant
defense system. The main sources of free radicals are represented by
hepatocyte mitochondria and cytochrome P450 enzymes, by endotoxinactivated
macrophages (Kupffer cells) and by neutrophils. In chronic
liver injury, the injured cells release a number of cytokines (Tipoe et
al., 2010). These cytokines then stimulate the Kupffer cells to release
more inflammatory mediators and various free radicals (Clària et al.,
2011). The presence of high concentration of these pro-inflammatory
mediators and free radicals then activities a large number of neutrophils
to release pro-inflammatory mediators and free radicals (Makni et al.,
2011).
One of sources of generation of reactive oxygen species (ROSs)
is CCl4. Carbon tetrachloride (CCl4) is frequently used to produce liver
injury in animals so it is used to evaluate the therapeutic potential of
drugs (Basu, 2011). CCl4 is responsible for oxidative stress and lipid
peroxidation through cytochrome P450-mediated generation of highly
reactive radicals, leading to eventual damage characterized by
hepatocellular necrosis (Gong et al., 2012).
Liver diseases often progress from sub-clinical icteric hepatitis to
necro-inflammatory hepatitis, fibrosis, cirrhosis and hepatocellular
carcinoma (Vitaglione et al., 2004 and Cristovao et al., 2007). Liverfibrosis is characterized by excessive accumulation of extracellular
matrix (ECM) proteins such as type I and type IV collagen within the
perisinusoidal space of Disse (Dai et al., 2009). It is a major feature of
most chronic liver injuries, including metabolic, viral, cholestatic and
biliary disorders (Pinzani and Rombouts, 2004; Haber et al., 2008
and Henderson and Forbes, 2008). Abnormal flow of bile acids and
bilirubin in the liver is characterized of cholestasis, which leads to
retention and accumulation of toxic hydrophobic bile salts within
hepatocytes (Faubion et al., 1999), causing inflammatory reactions,
hepatocyte death and periductular fibrosis (Webster and Anwer,
1998). Oxidative stress is likely to play a key role in cholestasisinduced
liver fibrosis, as evidenced by reduced liver injury and fibrosis
after bile duct ligation (BDL) in mice lacking NADPH oxidase (NOX-
1), which produces reactive oxygen species (ROSs) (Cui et al., 2011).
The cirrhosis of liver is a heterogeneous group of chronic,
progressive and irreversible diseases for which no satisfactory
treatment is available (Conn, 1975). All cases of cirrhosis are
characterized morphologically by the loss of normal liver architecture,
which is replaced by a new tridimensional structure based on the
combination of variable degrees of liver cell regeneration and excessive
connective tissue deposition (Popper, 1977). Cirrhosis produces
hepatocellular dysfunction and increased intra-hepatic resistance to
blood flow, which result in hepatic insufficiency and portalhypertension, respectively (Gines et al., 2004). Cirrhosis affects
hundreds of millions of patients world wide.
Modern medicines have little to offer for attenuation of hepatic
diseases and it is chiefly the plant based preparations which are
employed for the treatment of liver disorders (Somasundaram et al.,
2010). There is a great demand for the development of an efficient
hepatoprotective drug from the natural resources (Tandon et al., 2008).
Plants are rich source of bioactive components that have desirable
health benefits and are traditionally known to be useful for prevention
of chronic diseases. Many studies have reported that antioxidant
supplements are effective in preventing oxidative-stress-related liver
pathologies due to particular interactions and synergisms (Bhathal et
al., 1983 and Vitaglione et al., 2004).
Kidney diseases:
Kidney is a paired organ whose functions include removing
waste products from the blood and regulating the amount of fluid in the
body. The basic units of the kidney are microscopically thin structures
called nephrons, which filter the blood and cause wastes to be removed
in the form of urine. Together with the bladder, two ureters, the single
urethra and the kidneys make up the body’s urinary system.
Acute renal failure occurs frequently in critically ill patients in
intensive care (Nissenson, 1998). This disorder is defined as a sudden