INTRODUCTION:

Industrial and technological progress has been accompanied by the use of hundreds of chemical compounds in various industrial products that depend heavily on daily life such as chemical detergents, sterilizers, cosmetics, preservatives, dyes, plastic products, air fresheners, insecticides and other products that have become the title of civilization, progress, prosperity and prosperity. On a wide range of compounds and chemical elements, some of which may represent a real danger to the health and safety of those who are exposed, especially as many of them possess toxic and cumulative properties affecting the organs of the human body over a long period of time (1).

The risks of such compounds and toxic chemical agents are not limited to a specific organ in the human body, but affect all vital organs, but the specificity of the kidneys and liver and their sensitivity in the human body are made in the forefront of the organs of the body, which may be damaged and destroyed as it is difficult to repair such serious damage (2).

Cadmium is a toxic heavy metal with a density of five times the density of water (3). It is non essential trace metal and is found in very rare amounts of the body and its loss does not affect its vital functions (4) and that its high concentrations pollute the environment and threaten life (5) because it has the ability to disrupt ion exchange, thereby altering the permeability of the cell membrane (6).

There are severe effects of cadmium on the tissues of the body (7) having a half-life ranging between 15-35 year in the human body which increases its cumulative gravity (8) and is stored in the liver and kidneys (9) and is distributed in various tissues and organs such as the lungs, heart, brain, bones, muscles and genitals (10) causing liver damage (11), kidney damage (12), necrosis, dyspepsia (13), high blood pressure (14) and gastric mucus damage (7).

Due to the danger of cadmium and its negative effects on human health as it enters many industries related to humans, it enters the manufacture of batteries and dyes and rubber and plastic and cement, as well as in the manufacture of fluorescent lamps and welding wire and amalgam teeth and enter into the electroplating of various metals such as steel and aluminum and water pipes and reservoirs to cover the protective layer of erosion (15), this study was selected to study some of its histological and biochemical effects in males of white mice.

MATERIALS AND METHODS:

The study was designed at acentral animal house of college of Science, Babylon University.

Albino Mice:

The mice allowed into three cages applyingaphotoperiod 12 hr of light at 22±1.5 ˚C and humidity of Labrotary was saved between 47% to 56% during research, mice feding with control food belt.The weight of mice range between 25-27mg each experimental groups consist of six male mice over all 16 animals used in the experiment, including control group and treated groups. Mice given cadmium chloride (5,10) mg/kg and injected subcutenous for 40 days, while control group given a normal saline injected subcutenous for 40 days.

Biochemical parameters:

all parameters was measured in Reflotron-Roche-Germany.

Histological study:

The liver and kidney of albino mice were wased by normal saline and fixed rapidly in alcoholic Bouin ̛ s solution for one day and kept in 70% of ethyl alcohol. The specimens were processed for histological staining. The blocks were sectionedat5µm thickness and stained with routine stain (Haris Haematoxylin and Eosin) for histopathological effect study of cadmium chloride (16).

Statistical analysis:

all values of biochemicalstuding are allowed as means ±Standard error of means.Statics obtained were analysis by one-way analysis of variance (ANOVA) examination using the statistical package for Social Sciences (SPSS), and means have been designed by least significant difference (LSD).

RESULTS AND DISCUSSION:

Present study shown a significant increase (p>0.05) in the concentration of Got enzyme for treated groups (5,10)mg/kg when compared to control group ( Fig.1).

As for as the concentration of GPT enzyme we found a significant increase (P>0.05)for treated groups (5,10) mg/kg as a compared to control group( Fig.2) .

As forthe blood urea the studing shown a significant increase (p>0.05) in the concentration of urea and serum creatinine in treated groups (5,10) mg/kg as compared to control group ( Fig.3,4).and when compare between two groups we found difference but not significant and the differences increased with increase concentration of cdcl₂.

The histological study shownableeding,lysis, necrosis and hypertrophy in liver for treated groups as compared to control group (Fig.5).while in distal tubules of kidney shown lysis and increasing in lysis with increased the concentration of cdcl₂(Fig.6).

Figure 1: Refer to effect of cdcl₂ on the GOT in white male mice.

Figure 2: Refer to effect of cdcl₂ on the GPT in white male mice.

Figure 3: Effect of cdcl₂ on the blood urea in whitemale mice.

Figure 4: Effect of cdcl₂ on the serum creatinine in white male mice.

Figure 5: Sections in the liver of white male mice. (H and E stain, 400x) (a):control group showing central vein (CV) and normal hepatocytes with clear nuclei. (b): mice groups treated with cdcl₂(5mg/kg)showing bleeding (B),necrosis(N)and lysis (arrows).(c) mice groups treated with cdcl₂(5mg/kg) showing bleeding (B) and lysis(arrows).(d):mice groups treated with cdcl₂(5mg/kg)showing lysis (L) and hypertrophy (arrows).(e):mice groups treated with cdcl₂(10mg /kg) showing bleeding (B) and hypertrophy (arrows).(f): mice groups treated with cdcl₂(10mg/ kg) showing lysis(arrows).

Figure 6: Sections in the kidney of white male mice.(H and E stain, 400x). (a): control group showing normal tubules.(b): mice groups treated with cdcl₂(5mg/kg) showing lysis(L). (c): micegroups treated withcdcl₂(5mg/ kg) showing lysis(L). (d): mice groups treated with cdcl₂(10 mg / kg) showing lysis.

Many studies indicate that the liver is a very sensitive member of the toxic substances entering the body and is the place where the material is absorbed all by the bowel or direct to him through the blood (17) and the effect of these substances vary depending on the degree of toxicity and the dose of the body, Their risk increases with half their life in the fabric (18).

Many researchers have agreed that severe or chronic exposure to cadmium, whether with drinking water (19,20) or by diet (21,22) has led to increased liver enzyme activity (GOT) and (GPT) as this effect increases with increased dose and duration of exposure.

The results of the current study agreed with the results of the researchers mentioned above. Many researchers explained this increase to the effect of cadmium in changing the permeability of the membranes of the liver cells, which leads to the leakage of these enzymes to the blood and corresponds to this change with increased dose and duration of exposure (23) and necrosis of liver cells, which occurs as a result of the toxicity of certain substances or carcinogenic infiltration or liver cirrhosis leads to the leakage of these enzymes from broken cells and access to blood (24-26).

The results of the present study showed that there are toxic effects of cadmium chloride on the liver and kidney in male white mice, where a number of researchers reached the same results (27-29).

The liver is a sensitive member of the poisoning of cadmium as it accumulates for a long time in the tissues of the liver (30,31) because it contains the protein metallotrhionin, which is associated with cadmium after 6 hours of arrival to the liver (32,33) and complex composition CD-MT in the liver tissue as distributed to other tissues causing toxic damage to it (34,35).

The toxic effect of cadmium on the liver results in the inhibition of sulfalhydral groups and oxidative phosphorylation enzymes in the mitochondria, which lead to an increase over fatty oxides, liver congestion, hemorrhage, and oxygen deficiency, leading to Inflammatory cell infiltration such as neutrophils and kupffer cells that contribute to programmed apoptosis and hepatic cell necrosis as well as the direct toxic effect of free cadmium and its formation of free radicals that have the ability to alter liver function and structure (36-38).

It is clear from the results of the present study that the kidney is the target member of the damage of cadmium toxicity and attributed to the accumulation of free cadmium in the kidney responsible for the tubular necrosis and the destruction and death of epithelial cells, which is one of the most common causes of kidney failure (39) as it affects glomerular filtration with the possibility of direct toxic effect on cells within the tubules and oxidation of cellular lipid membranes (40) note that severe renal damage is possible to repair and the return of the tissue to normal on the dispute of chronic renal damage, which cannot then perform thenormal function of the tissue (41).

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Received on 01.08.2018 Modified on 17.08.2018

Research J. Pharm. and Tech 2019; 12(1): 99-102.

DOI: 10.5958/0974-360X.2019.00019.2