Abstract
Ultra-weak photon emission (UPE) of a living system received scientific attention because of its potential for monitoring increased levels of reactive oxygen species (ROS) in the pathogenesis of rheumatoid arthritis (RA). In this study, a highly sensitive cryogenic charge-coupled device (CCD) camera was used to monitor in a RA mouse model the photon emission both without and with luminol. For that purpose, arthritis was induced in mice utilizing a repeated co-administration of type II collagen with lipopolysaccharide. Quantitative imaging of ultra-weak photon emission of the front and back paws of the animals was initiated 70 days after the first injection. All of the animals were measured once without luminol and once again immediately after luminol injection. Data illustrated a higher UPE intensity after initiating arthritis by CII-injection of the animals. The increase in UPE intensity was measured with and without using luminol indicating that this imaging technology may be useful for the future study of human RA.
Highlights
Convincing evidence supports a role for oxidative stress and the subsequent production of reactive oxygen species (ROS) in the pathogenesis of many chronic diseases
When an excited carbonyl or singlet oxygen is released to the ground state, it can emit its energy as a photon in the visible range
Data illustrate a higher Ultra-weak photon emission (UPE) intensity at 70 days after initiating arthritis by CII- injection of the animals according to the procedure described [28]
Summary
Convincing evidence supports a role for oxidative stress and the subsequent production of reactive oxygen species (ROS) in the pathogenesis of many chronic diseases. The techniques that can be applied both non-invasively and locally estimating radiation energy vis-a-vis documentation of photon emission in the UV, visible and near IR ranges. Since the 1980’s, many experiments have revealed that weak photon emission could originate from natural biological reactions of free radicals and their derivatives, and from simple cessation of electronically excited states. One of the major sources of weak biological photon emission is mitochondrial oxidative metabolism and lipid peroxidation. It is due to the excited electrons of singlet oxygen 1O2 and carbonyl species R = O*. When an excited carbonyl or singlet oxygen is released to the ground state, it can emit its energy as a photon in the visible range. Emission occurring in deeper layers may be absorbed and become part of the transmission of excited states, both dark and light, the latter resulting in secondary radiation from other sources [7,8]
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