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Dr Malgorzata Rózanowska 

Staff Photos

Telephone:+44 (0)29 2087 5057
Fax:+44 (0)29 2087 4859
Location:Room 2.26, Maindy Road

Career Overview

After completing my PhD in 1998 at the Department of Biophysics, Faculty of Biotechnology, Jagiellonian University, Krakow, Poland, I continued my research and teaching at the same Department till September 2003 with two periods of research leave;

  • Travelling Research Fellowship (August 2000 - July 2002) awarded by the Wellcome Trust to work on a research project “Co-operation between Antioxidants in Protection of the Retina against Oxidative Damage” in collaboration with Professors Mike Boulton, School of Optometry and Vision Sciences, Cardiff University, Cardiff, UK, and T. George Truscott, School of Chemistry and Physics, Keele University, Keele, UK.
  • Senior Fulbright Fellowship (October 2002 – July 2003) to work on a project “Identification of the Molecules Responsible for Lipofuscin Phototoxicity” in collaboration with Professor John D. Simon, Duke University, Durham, NC, USA.

I joined the School of Optometry and Vision Sciences, Cardiff University as a lecturer on 1 October 2003.


 Research Interests

The general aim of my research is to better understand the mechanisms responsible for protection against photooxidative damage in the eye, especially in the retina. The outer retina is constantly exposed to high oxygen tensions and large concentrations of polyunsaturated lipids extremely susceptible to oxidation. Moreover, it contains several photosensitisers, that is molecules that upon absorption of visible light generate damaging reactive species such as singlet oxygen and free radicals. The protective mechanisms against photo-oxidative damage are extremely efficient in the retina. For most of us the retina performs its function properly throughout the whole lifetime. Only during the exposure to intensive light, such us during gazing directly at the sun, watching solar eclipse without proper filters, sometimes during eye surgery, these mechanisms fail and the retina becomes damaged.

Increased chronic exposure to blue light has been identified as one of the risk factors for development of ARMD – the leading cause of blindness of people above 60. About 30% of people above the age of 60 develop at least first signs of the disease but its etiology is not really known. It is not known how to prevent development of ARMD leading to the loss of vision. One of the hypothetical mechanism to prevent ARMD is to prevent oxidative damage to the retina by providing efficient antioxidant protection.

Retinal (vitamin A aldehyde)
One of photosensitisers present in the retina is all-trans retinal that accumulates in photoreceptor outer segments due to photobleaching of visual pigment, rhodopsin. Below photoreceptors there is a monolayer of retinal pigment epithelial (RPE) cells. Due to interactions between photoreceptors and RPE, retinal may impose a risk of photo-oxidative damage to RPE cells as well. The best protection against all-trans retinal-mediated photoreactivity would be to disable photogeneration of reactive oxygen species. And this is something that really happens in the retina, where most of the retinal remains bound to proteins and lipids, and the binding reduces its photochemical activity.

Antioxidant protection against oxidative damage
There is a number of endogeneously synthesized and dietary antioxidants, that may protect from reactive oxygen species. Carotenoids, such as those constituting macular pigment – lutein and zeaxanthin, effectively quench singlet oxygen in a safest way possible – they accept the excess energy from oxygen molecule and dissipate it thermally. Antioxidants react with radicals but as a result they become radicals themselves, which accumulation may have pro-oxidant effects. Antioxidants may increase their protective effects if present as a right combination, such as a combination of a singlet oxygen quencher (carotenoid) and a free radical scavenger (vitamin C or vitamin E), which offer better protection against photo-oxidative damage than increasing concentrations of individual antioxidants.

Melanin is a dark pigment in the eye and skin, synthesised in the skin during tanning. Melanin constitutes the major pigment in young RPE cells is, where it is present within melanosomes. Although melanin is photoreactive, its prooxidant potential is significantly smaller compared to all-trans retinal or lipofuscin. Only in the presence of ascorbate, aerobic photoexcitation of melanin induces substantial generation of superoxide anions and hydrogen peroxide. Due to optical screening, sequestration of metal ions, free radical scavenging and quenching of excited states of photosensitisers, melanin exhibits antioxidant properties. Melanin can also 'repair' oxidised carotenoids by efficient electron transfer. However, melanosomes undergo age-related changes – their photoreactivity increases with age; the total melanin concentration and number of melanosomes decreases; and there is age-related increase in a number of complex granules – melanolysosomes and melanolipofuscin.

Lipofuscin, so called age pigment, that accumulates in different tissues with ageing.In the retina, lipofuscin is believed to be formed from incomplete digestion of photoreceptor outer segments, which are constantly shed and phagocytosed by RPE. Retinal lipofuscin is easily visible in older human eyes due to its characteristic golden-yellow fluorescence. Lipofuscin is at least in part responsible for the age-related increase in the susceptibility of RPE cells to photooxidation. Lipofuscin, which upon excitation with visible light generates several reactive oxygen species: singlet oxygen, superoxide anion, lipid hydroperoxides and hydrogen peroxide. My results indicate that singlet oxygen if formed by energy transfer from excited triplet state of a non-polar photosensitizer(s) present in lipofuscin. Photoexcited lipofuscin leads to oxidation of lipids and proteins. The observed photoreactions of lipofuscin are wavelength dependent, being more pronounced at shorter wavelengths.However, it is still unknown what the identity of the photosensitizer(s) within the lipofuscin granule is. Our recent data indicate that it may be the products of peroxidation of docosahexaenoic acid, the most unsaturated fatty acid in mammals; however, it still remains to be determined which are the ones out of the hundreds formed. We do not really know why lipofuscin is formed and whether we can prevent its accumulation. In the hypothetical mechanism of lipofuscin formation the central role plays retinal. Due to its photoreactivity, it may induce oxidation of lipids and proteins in rod outer segments, and makes them resistant to lysosomal degradation.

In my studies I use direct electron spin resonance (ESR) spectroscopy, ESR oximetry and spin trapping, nanosecond laser flash photolysis, time-resolved detection of characteristic phosphorescence of singlet oxygen at 1270 nm, pulse radiolysis, and fluorescence and absorption spectroscopy. To study (photo)toxicity and antioxidant protection against (photo)oxidative damage, I use cells in culture and standard tests of cell function and viability.