We are IntechOpen, the world's leading publisher of Open Access books Built by scientists, for scientists

4,500+

Open access books available

119,000+

International authors and editors

135M+

Downloads

151 Countries delivered to Our authors are among the

Top 1%

most cited scientists

12.2%

Contributors from top 500 universities

Selection of our books indexed in the Book Citation Index in Web of Science™ Core Collection (BKCI)

## Interested in publishing with us? Contact book.department@intechopen.com

Numbers displayed above are based on latest data collected. For more information visit www.intechopen.com

## Meet the editor

Professor Mahmoud Mansour is currently a Professor of biochemistry at the College of Pharmacy, King Saud bin Abdulaziz University for Health Sciences. He received his pharmacy degree from the Al-Azhar University Cairo, Egypt in 1984, and his PhD degree in clinical biochemistry from the Karolinska Institute, Stockholm Sweden in 1992. From 1996 to 2016, he joined the King Saud University. As a fellow, he has contributed significant-

ly to defining some aspects of the molecular biology of tissue injury and induction of liver and renal toxicity, with particular focus on the role of antioxidants in the prevention and treatment of different toxic effects. In addition, he has contributed notably to developing a new strategy for tumors especially in the liver. His research has shown that the proteasome inhibitor plays an important role in preventing carcinogenesis of the liver by metastatic tumors. He then moved to King Saud bin Abdulaziz University for Health Science, where he continued to work on the pathogenesis of cancer and on issues concerning the cellular and molecular mechanisms of cancer biology and the metastatic process. He is now conducting studies on liver cancer using gankyrin.

Contents

*by Mahmoud Ahmed Mansour*

Adenocarcinoma Cells In Vitro

*Damir Đermić and Hrvoje Mazija*

*by Marija Vavlukis and Ana Vavlukis*

*by Bukem Tanoren Bilen*

**Preface III**

**Chapter 1 1**

**Chapter 2 7**

**Chapter 3 29**

**Chapter 4 43**

**Chapter 5 65**

**Chapter 6 77**

**Chapter 7 101**

*by Abubakar Babando Aliyu, Jonathan Ilemona Achika, Joseph Adesina Adewuyi,* 

Royal Jelly and Human Interferon-Alpha (HuIFN-αN3) Affect Proliferation,

*by Arunachalam Muthuraman, Narahari Rishitha, Nallupillai Paramakrishnan,* 

Introductory Chapter: Free Radicals and Lipid Peroxidation

*Bhaskaran Mahendran and Muthusamy Ramesh*

Lipid Peroxidation in Meat and Meat Products *by Ana Lúcia F. Pereira and Virgínia Kelly G. Abreu*

Role of Lipid Peroxidation Process in Neurodegenerative Disorders

Antioxidants from Nigerian Medicinal Plants: What Are the Evidence?

*Patience Gangas, Hamisu Ibrahim and Adebayo Ojo Oyewale*

Atherosclerotic Cardiovascular Disease Protection

Designating Vulnerability of Atherosclerotic Plaques

Glutathione Level, and Lipid Peroxidation in Human Colorectal

*by Bratko Filipič, Lidija Gradišnik, Klemen Rihar, Adriana Pereyra,* 

Statins Alone or in Combination with Ezetimibe or PCSK9 Inhibitors in

## Contents


Preface

Lipid peroxidation is the major molecular mechanism that induces oxidative damage to cell structures and is also involved in the toxicity process that leads to cell death. Lipid peroxidation was initially studied as a mechanism for the damage to alimentary oils and fats; however, others thought that lipid peroxidation was the consequence of toxic metabolites (e.g. CCl4) liberating a highly reactive species, the carbon trichloride methyl radicals (CCl3). This radical quickly adds molecular oxygen to form the trichloromethylperoxy radical. Removal of hydrogen atoms from unsaturated fatty acids by such radicals creates carbon-centered lipid radicals. These radicals quickly add molecular oxygen to form lipid peroxyl radicals, thereby, initiating the process of lipid peroxidation. Unless scavenged by radical scavengers, these lipid peroxy-radicals in turn abstract hydrogen

atoms from other lipids molecules, thereby initiating the process of lipid

Lipid peroxidation is a chain reaction initiated by the hydrogen abstraction or addition of an oxygen radical, resulting in the oxidative damage of polyunsaturated fatty acids (PUFA). PUFAs are more sensitive than saturated fatty acids because of the presence of a double bond adjacent to a methylene group that makes the methylene C-H bond weaker and therefore the hydrogen is more susceptible to abstraction. This leaves an unpaired electron on the carbon, forming a carboncentered radical, which is stabilized by a molecular rearrangement of the double bonds to form a conjugated diene, which then combines with oxygen to form a

In pathological situations the reactive oxygen and nitrogen species are generated at higher than normal rates, and as a consequence, lipid peroxidation occurs with deficiency of endogenous antioxidants as alpha-tocopherol deficiency or reduced glutathione. In addition, in the presence of high concentrations of PUFAs and transition metals, biological membranes of cells and organelles are constantly being subjected to various types of damage. The mechanism of biological damage and the toxicity of these reactive species on biological systems are currently explained by the sequential stages of reversible oxidative stress and irreversible oxidative damage. Oxidative stress is understood as an imbalance between increased oxidants or decreased antioxidants. The concept implies the recognition of the physiological production of oxidants (oxidizing free radicals and related species) and the existence of operative antioxidant defenses. The imbalance concept recognizes the physiological effectiveness of the antioxidant defenses in maintaining both oxidative stress and cellular damage at a minimum level in physi-

peroxidation.

peroxy-radical.

ological conditions.
