The normal growth of liver (control group, C)
This study revealed the general structure of the liver, which is formed of DC and PC. The DC are characterized by the presence of many cytoplasmic organelles and relatively variable nuclei (N) with dark chromatin. However, PC contain more abundant RER and free R and their N are true with equally distributed chromatin.
This agrees with Bourne  who also described that the liver contains KC, EC that line BS, and parenchymal cells which are divided into DC and PC. Also, Medlock and Haar  and Abdel-Fatah  stated that cytoplasm of DC contains large number of Mi, RER, primary lysosomes (LY1), secondary lysosomes (LY2), lipid droplet (LD), and Golgi apparatus (G), with less smooth endoplasmic reticulum (SER).
The N of hepatocytes are large, surrounded by NE, and contain two types of nuclear chromatin (ECr and HC). In agreement with our results, Abdel-Fatah  and Bruni and Porter  reported that N contain two types of chromatin, HC and ECr, and that they are surrounded by double layered nuclear membrane that contains many NP spread over variable distances.
All the cytoplasmic organelles appeared in the liver cells of our study including RER and R. This is consistent with Moule  who recorded that the liver cells at the age of 8 days of incubation showed RER and R which are scattered in the cytoplasm. Bruni and Porter  reported that there is difference in the position of endoplasmic reticulum (ER) not only from one liver cell to another, but also in a single liver cell, which indicated that ER is not a standard compound, but there may be changes in its direction, position, or composition. They also showed that SER are distributed in areas of the cell rich in glycogen (GL).
The G appeared to have two faces (FF and MF) and contain. It was located around the N, near BC and the BS. This description was corroborated by Abdel-Fatah , Johnson , Al-Yousuf , and Burkitt et al.  who described G as a group of cisternae and parallel V with many gaps, and that they have two sides, convex and concave, and lie very close to the N, BC, and BS.
The Mi appeared with variable shapes and sizes. It had two membranes separated by a space, where the inner membrane was folded inwards to form cisternae. It was spatially associated with the RER. This is consistent with Bruni and Porter  who reported that Mi are closely related to RER. Al-Yousuf  and Burkitt et al.  added that Mi are variable in size but mostly rectangular, and their number may reach up to 2000 per cell.
The lysosomes appeared in their various types which include Ly1, Ly2, P, and MB. This agrees with Bruni and Porter  and Burkitt et al.  who reported that LY1 appeared as membrane-bounded organelles, variable in size and shape, and contained undifferentiated granular materials, while LY2 were more variable in their appearance and some of them were very dense. Moreover, P appeared as small spherical membrane bounded structures.
Glycogen particles were seen collected in the cytoplasm near SER. Also, Han and Holmsted  noted that SER are closely related to GL particles. However these particles are rare or completely absent in areas of RER and/or R.
LD of variable sizes were detected in the liver cells of this study. This agreed with Abdel-Fatah  and Mahmoud  who described LD as multi-form fatty globuli of variable sizes.
BC regions were seen between adjacent cells. The plasma membranes of the cells close to BC were bound by tight bonds which include (ZO), (ZA), and D junctions. This result was supported by Han and Holmsted  who reported that BC are areas between the membranes of adjacent hepatocytes.
In this study samples, the hepatic cells were separated by BS lined with EC and KC. The EC lining BS were separated from liver cells by a space called DS. Bruni and Porter  explained that blood fluids pass freely through EC of BS to DS to be in direct contact with the hepatic cells facilitating the exchange of important substances between blood and hepatic cells.
The effect of monosodium glutamate on the structure of the liver of chicken embryos (MSG group)
Many structural changes had occurred in the liver cells after exposure to MSG. The changes that occurred in N included irregular NE, dilatation of NP, or increased HC. Moreover, many N have lost their electron density. This agree with Farhoud  and Abdel-Fatah  who reported that the changes occurred in N of liver cells of chicken embryos included increase in HC amount and disturbance of its distribution. Also, the NE became irregular and interrupted with expansion of space between its two layers and dilatation of NP with some connection between nuclear material and cytoplasm.
Major changes have occurred in mitochondria where their envelope became irregular and their components get degraded. These results are supported by Abdel-Fatah  who reported appearance of abnormal Mi, which were either decayed, partially or completely atrophied with disruption of its components, increase of its density, and deposition of decayed materials inside it. Hummdi  indicated that the marked changes that occurred in Mi, including its atrophy or deposition of decayed materials inside it, resulted in loss of its functions and damage of the cell.
The RER showed fragmentation, vacuolation, and dilation in some of its parts. This agrees with the results of Abdel-Fatah  who confirmed that one of the most prominent observations on RER was its appearance either fragmented or vacuolated with disturbances in its shape. Also, it sometimes appeared decayed and free of R.
SER showed proliferation of its units and disturbance of its distribution. The proliferation of SER might be explained by its ability to detoxify MSG. This is consistent with Moody and Reddy  and Ahmed  who reported a close association between the proliferation of SER and the degree of cell damage. Ayman et al.  explained the increase in SER proliferation as a rapid response to the adverse effects on cells and that it is associated with an increase in enzymes’ activity to increase the cells ability to detoxify harmful substances.
The G appeared as either atrophic or hypertrophied bodies with expanded or vacuolated membranes.
This can be explained by that G are organelles characterized by its rapid decay and that they are difficult to be detected. This observation was supported by Abdel-Fatah  who reported that G were difficult to be distinguished. They were found inside hepatic cell in the form of either atrophied or hypertrophied bodies and often appeared near the nucleus or the edges of hepatic cell adjacent to BC.
Our samples showed variable distribution of LY1, LY2, and P inside the treated cells, and some of them appeared attached to LD or contained reactions products. This agrees with Ahmed  and de Duve  who reported increase in LY numbers and hydrolysis with release of LY enzymes such as phosphatase secondary to cell injury.
BC appeared as dilated areas with short MV. Also, there was decrease in their numbers and increase in the number of desmosomal junctions surrounding the multiplied BC. This is supported by Abdel-Fatah  results which showed that during acute injury of hepatic cells, the D appeared wide, proliferated with distortion of their composition.
BS were extensive with destruction of their walls and enlargement of their lining cells. The BS cavity appeared filled with RBCs, cellular residues, and collagen fibers. This agrees with the observations of Hassan  and Cotran  who attributed the enlargement of KC to defensive activity of these cells against poisoning. Abdel-Fatah  and Eid et al.  emphasized that BS appeared dilated and more extended with presence of many cellular residues, collagen fibers, broken MV, and dead cells inside their cavities.
There was variable sized cytoplasmic vacuoles in MSG-treated liver cells as reported also by Pfeifer and Bannasch , Tuchweber et al. , and Abbasi et al. . These vacuoles may be caused by mitochondrial swelling or decomposition of mitochondrial remnants as reported by Takano et al , or due to enzyme digestion of cell organelles due to cell injury as reported by Cotran , Biondo-Simões et al. , Aldana et al. , and Luty et al. . Also, Bourne  reported that formation of these vacuoles may be a part of defensive mechanism to prevent interference with cell vital activities or may be due to sinusoidal dilatation as reported by Shibayama et al. . The membrane surrounding these vacuoles showed the same enzymatic activity of liver cell membrane; so many scientists believe that they are indentations from cell membrane. Tuchweber et al. , Takano et al. , and Burkitt  reported that these vacuoles are LD that accumulated secondary to obstruction of fatty acids metabolism by liver cells.
There were excessive collagen fibers in connective tissues and between liver cells of our samples. This agrees with Farhoud  who reported large amount of collagen fibers in the base plate of the mouse at 3rd week of MSG injection. Awad  added that the amount of collagen fibers in connective tissues barriers and among cells was more or less than control sample on days 10–12 of preparation, and as growth advanced at 15–18 days of preparation, there was an increase in the amount of collagen fibers in barriers between cells.
Also there were a few GL particles in the MSG-treated cells and this was also observed by Dixon et al.  who found depletion of GL from cells.
There was expansion in the intercellular (IS) spaces with associated expansion of BS. This was confirmed by Young  who reported that intercellular expansion is a common phenomenon associated with BS expansion and resulted from fluids accumulation between cellular components as collagen fibers.
The changes that occur in the cellular functions as a result of the toxic compounds include changes in cell membrane permeability and affection of movement of materials to and from the cells. They also include changes in cellular enzymatic activities, changes in cellular division rates, changes in DNA and protein synthesis, changes in cell respiratory processes rate, and changes in energy molecules availability. Al-Ghamdi  reported that the harmful effects of the toxic chemicals may be caused by binding of these toxic chemicals to the biomolecules. This binding may be reversible or irreversible leading to apoptosis or affection of the cellular structure.
The effects of MSG on liver tissues can be explained by its ability to infiltrate and cross blood-brain-barrier due to incomplete development and weakness of this barrier, especially in fetuses, newborns and infants, causing high toxicity followed by defects in growth and differentiation of various tissues and cells. It also induces neurotoxicity by interacting with N-methyl-D-aspartate (NMDA) receptors causing inhibition of membrane proteins formation and change of the cell membrane organization causing cell destruction.
Burkitt et al.  explained that cellular decomposition occurs secondary to the inflammatory reactions of body’s immune system against damage caused by chemical compounds, parasitic and viral infections, and harmful substances.
Overstreet et al.  concluded that MSG had ability to cross epithelial cells membranes in peritoneal cavity and break down into sodium and glutamic acid where some of glutamic acid is excreted and the rest is converted into glutamate and during this process, the liver cells try to repair the damage occurred in their organelles. With the high percentage of glutamate, the liver cells cannot excrete or detoxify it, so a series of hemolytic changes occurs in liver gradually and finally death of the liver cells occur. Anbarkeh et al.  reported that cytotoxicity (apoptosis) may occur due to many factors as DNA damage, loss of survival signals, or oxidative voltage. Giorgio et al.  said that apoptosis occurred when the cell was severely injured as cell swells and ruptures and these effects occur because the injury prevents the cell from adjusting balance of its fluid and ions that are usually pumped out of the cell but in case of infection, they flow into cells.
Anindita et al.  and Hassan et al.  reported that MSG administration resulted in significant changes in apoptotic biomarkers as programmed cell death protein-1 related to liver damage and decrease in hepatic cell thickness.