Most metal ions have oxidation and antibacterial
effect. In old days, heavy metal has been used for preserving food and antibacterial
treatment very early. The order of antibacterial power is as following:
Ag+ > Hg2+ > Cu2+ > Au2+
> Zn2+ > Ca2+ > Na+. According
to chemical elements, the Ag ion with positive charge among the metal has
the biggest deoxidizing power. It can sterilize and has a specified duration,
so it is used for developing antibacterial technology. So using Ag ion is
feasible in technology. The antibacterial order is: Ag3+ >
Ag2+ > Ag1+. Different Ag with different valences
has different antibacterial characters. In general, Ag2+ has
a antibacterial characters as 50-250 times as Ag1+.
Active
antibacterial mechanism of zinc ions:
The reaction mechanism of zinc ions and bacterium:
After bacteria are killed, Zn2+ comes
out and contact with other bacterium, and start to kill them
once again. So zinc oxide has been used in woundplast as antibacterial
material and wound astringent abroad, and has a good effect.
Active antibacterial mechanism
of Ag ions:
The antibacterial mechanism of catalysis: The
Ag ion catalysis causes the common ingredients of microbes broken
or function obstacle. When trace Ag ions get to microbes’
membrane, because the membrane carries with negative ions, which
absorbs Ag ions hard depending on coulomb gravitation, so Ag
ions can penetrate cell wall and enter it, then react with SH
group and make protein solidified. It breaks the activation
of cell composing enzyme and make cells dead for losing division
and multiplication functions. Ag ions also can break microbes’
electronic transmitting system, respiratory system and matters
transmitting system.
Antibacterial mechanism of Ag ions as following:
The microbes such as bacterium and mildew take
with negative charge, and antibacterial ions take positive charge.
When the microbes clinging to glass surface contact with Ag+,
the cell wall is penetrated and broken according to coulomb
gravitation. The Ag ions contact with protein, lose its activation
and finish the process of restraining and extinguishing bacterium.
Ag+ itself isn’t consumed after killing the
cells and doesn’t lose the power of killing new bacterium.
The slow-releasing and
sterilization mechanism of Ag ions
The slow-releasing and sterilization mechanism
of Ag ions means antimicrobial releases Ag+ slowly as using.
Because Ag+ can break microbes’ cell membrane
or absorb SH group in enzyme protein strongly under low concentration,
combine with it quickly, and decrease the activation of active
enzyme, so it has a antibacterial effect. By releasing Ag+
slowly, abio-antimicrobial can play a long-term antibacterial
effect. The reaction process is as following:
The sketch map of Ag+ sterilization process is
as figure 1.
So it is obvious that Ag+ only can
kill bacterium but decompose and clear bacterium remains.
2.3 Active oxygen antibacterial mechanism of Ag
ions
The mechanism is: the reduction potential of Ag
at high oxidation state is very high. Under the light, antimicrobial
react with water or air, producing active O2- and
·OH, which has strong redox.
In fact, the basis of composing microbes’
cell membrane is fat, mostly is phosphatide.
Phosphatide molecules constitute hydrophile head basing on phospho
and choline phosphate, which are distributed outside the cell
membrane; discharging tails constituted with the neutral discharging
group of long-chain fatty acid alkyl. The tails are distributing
in the core of membrane. The length of long-chain fatty acid
alkyl and the quantity of double bond can affect the characters
of membrane. So that when microbes close up antibacterial materials,
O2- and ·OH produced besides antibacterial
materials will attack cell membrane, and cause the results:
(a) The a-helix content in the secondary structure of token
protein has changed; (b) 1727cm-1 IR apex strength of c=0 double
bond has increased, and the tropism of glyceryl framework has
changed; (c) c=0 gene near polar section has increased; (d)
c=0 double bond has reduced, unsaturation of hydrocarbon chain
has decreased; (e) the secondary struction of membrane protein
is difficult to resume after damage, and the damage is not reversible.
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