Conceptual Framework Explanation

Rats exposed to CCl4 in their body, then CCl4 metabolism takes place in the

endoplasmic reticulum of liver cells and will produce a reactive substance which is CCL3.

CCl4 toxicity begins with the conversion of CCl4 molecules to CCl4 free radicals by

cytochrome P450 (Robbins & Kumar, 1995). CCl₃ free radicals will react with oxygen to

form a highly reactive trichloromethyl peroxide (CCl₂O ) that highly reactive (Hodgson &

Levi, 2000). These free radicals will react with polyunsaturated fatty acids which are

important components of the cell membrane and produce lipid peroxidation (Robbins &

Kumar, 1995).

CCl₃O₂ is highly reactive to biomolecules such as proteins, lipids, carbohydrates and

nucleotides. This highly reactive free radical will cause an increase in ROS. Increased ROS

causes lipid peroxidase. This increase in lipid peroxidase causes a decrease in GSH levels.

If the number of free radicals exceeds the amount of endogenous antioxidants, lipid

peroxidase initiation occurs which results in a decrease in GSH which is the GSHpx enzyme

substrate.

Increased lipid peroxidation causes the activation of the enzyme GSH peroxidase to

decrease, resulting in damage to proteins, DNA and phospholipids. By giving exogenous

antioxidants in the form of vitamins C and E, it is expected to optimize the activity of GSH

peroxidase enzymes, thus inhibiting cell damage.