PPT on Degenerative Diseases

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Transcript of PPT on Degenerative Diseases

ANTIOXIDANTS IN DEGENERATIVE

DISEASES

By,Dr. Ramesh C.K,Associate Prof & chairman,Dept of Biotechnology,Sahyadri Science College (Auto) Shivamogga -577203, Karnataka, India.

Diseases

non infectiousInfectious

What is a disease? Disease is a disorder or malfunction of the mind or body,

which leads to a departure from good health What are type of diseases?

Infectious

Bacteria

Viruses

Protozoa

Fungi

Simply saying diseases that are caused by pathogens

Non Infectious

Cancer

Diseases that are not caused by pathogens

Mental diseases

Schizophrenia &

Parkinson’s

Alzheimer’s disease

Cardiovascular

Heart failure

Atherosclerosis

Ischemic heart disease

Sarcoma

CarcinomaLung

cancerLeukemi

a

Oxidants are Oxygen free Radicals or those molecules with lone pair of electron

They are produced in normal metabolism of cell and also by environmental pollutants . They are very unstable ready to grab electron from surrounding system.

Oxidants and their relation in diseases

How do they produced in the cell ?

What are the targeting sites by the Free radicals ?

In cells (mitochondria), Electrons can leak from the mitochondrial respiratory chain, attach themselves to molecules and form free radicals. These free radicals target cell components and damage the cells (Trouillas et al., 2003). Creating a stress condition in cell, if untreated than lead to diseased condition

ROS

Lipid (peroxidation)

Protein (Thiol

oxidation)

DNA (hydroxyl DNA compounds)

Cell Damag

e

Targets on

Lipid peroxidation

Unsaturated fatty acyl

Malonyldialdehyde

And TBARS

Oxidative stress

Reference (Locatelli et al., 2003).

Hydroperoxides

Oxidation effect on Lipids (peroxidation)

Tau protein is very important in stabilizing the Neurons by pairing with never cells, In AD, tau begins to pair with other threads of tau and they become tangled up together. The defective tau, however, appears to block the actions of the normal microtubules. When this happens, the microtubules disintegrate, collapsing the neuron’s transport system. This may result first in malfunctions in communication between neurons and later in the death of the cells.

Beta amyloid formation is also important phenomena in alzheimer’s, Amyloid precursor protein (APP) is a large nerve-protecting protein, helps neurons to grow and survive. APP may help damaged neurons repair themselves and may help parts of neurons grow after brain injury. In AD, certain enzymes, particularly those called gamma-secretases, slice APP into pieces called beta amyloid. This process is controlled by factors called presenilin proteins. High levels of beta amyloid are associated with reduced levels of the neurotransmitter acetylcholine. ERAB (endoplasmic-reticulum associated binding protein) appears to combine with beta amyloid, which in turn attracts new beta amyloid from outside the cells. High amounts of ERAB may also enhance the nerve destructive power of beta amyloid. As beta amyloid breaks down it releases unstable chemicals called oxygen-free radicals. Once released, oxygen-free radicals bind to other molecules through a process called oxidation. This free radical can cause adverse effect.

Living organisms have evolved antioxidant defenses to remove excess free radicals

Exam- Superoxide dismutases, Catalase, glutathione peroxidases and etc But only these are not enough to control the ROS so dietary in take of antioxidants

Antioxidants

Super oxide dismutase plays a major role in the firstline of the antioxidant defense system by catalyzing thedismutation of superoxide radicals to form hydrogenperoxide and molecular oxygen. Mechanism of catalaseprovided by SOD suggests, that this enzyme is incompleteantioxidant, which prevent the superoxide anion andproduces the other. Its biological action is connected w ithcatalase via H2O2. Catalase is a ubiquitous enzyme presentin cells of aerobic organism. Catalase converts twomolecules of the strong oxidant, hydrogen peroxide tomolecular oxygen and two molecules of water(Laszlo et al., 1991). Kono et al. (1982) found thatsuperoxide anion inhibited these catalase action and thepresence of hydrogen peroxide inhibited the action ofdismutase.