Skip to main content
Malgorzata Rozanowska

Dr Malgorzata Rozanowska

Senior Lecturer

School of Optometry and Vision Sciences

Available for postgraduate supervision


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 Overview

My research is focused on understanding the mechanisms responsible for the light-induced damage to the retina, and the major factors contributing to the increased oxidative stress in the ageing retina, and in age-related macular degeneration (AMD), as well as the defence mechanisms involved in protection of the retina against oxidative damage. The understanding of these mechanisms can contribute to the development of effective prophylactic and/or therapeutic treatments for AMD.

Teaching Overview

  • Module Leader OP1206 Ocular Anatomy and Physiology
  • Lectures in OP1206 Ocular Anatomy and Physiology, OP1205 From Cells to Systems, and OP3207 Research in Optometry and Vision Science
  • Supervision of the practical components of OP1206 Ocular Anatomy and Physiology
  • Supervision of third year project students
  • Supervision of PhD and MSc students.
































  • Sarna, T. and Rozanowska, M. B. 1994. Phototoxicity of the eye. In: Jori, G. ed. Photobiology in Medicine. NATO ASI series. Series A, Life sciences Vol. 272. New York, NY: Plenum Press, pp. 125-141.



Book sections



The general aim of my research is to better understand the sources of oxidative damage, and mechanisms responsible for protection from oxidative 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.

An increased chronic exposure to light has been considered as one of the risk factors for development of age-related macular degeneration (AMD) 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 aetiology is not clear, and the therapeutic options to delay vision loss are limited.

In my research, I investigate mostly the roles in the retina of mitochondria, melanosomes, and lipofuscin granules as well as small molecules such as retinoids, carotenoids, polyunsaturated fatty acids, and how they can affect retinal function and development of AMD.

Endogenous retinal photosensitizers and photoprotectants

Retinaldehyde (vitamin A aldehyde) One of photosensitizers present in the retina is all-trans-retinaldehyde, a reactive aldehyde, which accumulates in the photoreceptor outer segments due to photobleaching of visual pigment, rhodopsin. Upon exposure to UV or blue light, all-trans-retinaldehyde generates reactive oxygen species, such as singlet oxygen, and undergoes photodegradation. The photodegradation products retain photoreactivity of all-trans-retinaldehyde and exhibit greater toxicity and phototoxicity than all-trans-retinaldehyde. In the intimate proximity to the photoreceptor outer segments, there is a monolayer of retinal pigment epithelial (RPE) cells. Due to interactions between the photoreceptors and RPE, all-trans-retinaldehyde may impose a risk of photo-oxidative damage not only to photoreceptors but also to the RPE cells. In my research, I test the hypothesis that all-trans-retinaldehyde is the major factor responsible for the acute light-induced damage to the retina, as well as for the accumulation of lipofuscin, which then propagates the chronic damage.

Hypothetical pathways by which all-trans-retinaldehyde (atRal) accumulated in photoreceptor outer segments (POS) as a result of photobleaching of visual pigments leads to photodamage of photoreceptors and retinal pigment epithelium (RPE): AtRal can mediate the generation of superoxide radical anion (O2 ), and O2 singlet oxygen (1O2), and peroxides (ROOH) when irradiated with UV or blue light. Unless effective antioxidants and repair enzymes counteract it, these reactive oxygen species produced by atRal can induce oxidative damage to lipids and proteins, which may affect their structures and functions, including inactivation of enzymes involved in atRal removal. The tips of the outer segments are phagocytosed daily by the RPE, and are meant to undergo lysosomal degradation. However, oxidatively damaged lipids and proteins may no longer be susceptible to the degradation by lysosomal enzymes, and/or may inactivate the enzymes. As a result of incomplete lysosomal degradation of the outer segments, the residual bodies, called lipofuscin (LF) accumulate in the RPE. LF photoactivated by blue or green light can also generate reactive oxygen species, and induces further oxidation of intragranular components, some of which may leak out of the granule and cause damage to the cellular components of the RPE, leading to RPE dysfunction or even death. Some of the oxidation products affect gene expression in the RPE, resulting in a release of pro-inflammatory and pro-angiogenic cytokines. The exocytosed lipofuscin may contribute to the formation of age-related deposits, such as drusen, accumulating between the RPE and Bruch's membrane, which separates the RPE from the choroidal blood supply. Some components of those deposits exhibit photosensitizing properties and include oxidation products with pro-angiogenic and pro-inflammatory properties. Moreover, oxidation leads to formation of crosslinks in the Bruch's membrane contributing to loss of its permeability.  For more, please see:

Lipofuscin, also called an age pigment, accumulates in different tissues with ageing. In the retina, lipofuscin is believed to be formed from an incomplete digestion of photoreceptor outer segments, which are constantly shed and phagocytosed by the RPE. Retinal lipofuscin is a mixture of lipids, highly modified proteins, photosensitizers and fluorophores. The fluorophores make the lipofuscin easily visible in human eyes due to its characteristic golden-yellow fluorescence. The photosensitizers make the lipofuscin at least in part responsible for the age-related increase in the susceptibility of RPE cells to photooxidation. Upon excitation with visible light, an unknown photosensitizer of lipofuscin undergoes an intersystem crossing to form a triplet state. In the presence of oxygen, the energy of the triplet state is transferred to oxygen resulting in generation of an excited state of molecular oxygen, singlet oxygen. In addition to generation of singlet oxygen, lipofuscin generates other reactive oxygen species: superoxide, lipid hydroperoxides and hydrogen peroxide. Photoexcitation lipofuscin leads to oxidation of lipids and proteins, both intra- and extragranular. The observed photoreactions of lipofuscin are dependent on the irradiation wavelength, being more pronounced at shorter wavelengths. However, it is still unknown what the identity of the photosensitizer(s) within the lipofuscin granule is.


Melanin is a dark pigment of the eye, hair and skin. In the skin, melanin is synthesised mostly in response to exposure to UV-A light. In the eye, melanin synthesis starts early during foetal development and is completed within a few years after birth. Melanin constitutes the major pigment in young RPE cells is, where it is present within melanosomes. Although melanin is photoreactive, its pro-oxidant 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 and hydrogen peroxide. Due to the 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 an efficient electron transfer. However, melanosomes undergo age-related changes and their photoreactivity increases with age. As we age, the total melanin concentration and number of melanosomes decreases in the RPE; and there is age-related increase in a number of complex granules melanolysosomes and melanolipofuscin.

Antioxidant protection against oxidative damage

In addition to melanin and retinoids, there is a number of endogeneously synthesized and dietary antioxidants, which may protect the retina 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, accumulation of which 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.

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 established tests of cell function and viability.


Teaching Overview

  • Module Leader OP1206 Ocular Anatomy and Physiology
  • Lectures in OP1206 Ocular Anatomy and Physiology, OP1205 From Cells to Systems, and OP3207 Research in Optometry and Vision Science
  • Supervision of the practical components of OP1206 Ocular Anatomy and Physiology
  • Supervision of third year project students
  • Supervision of PhD and MSc students.


Educational and Professional Qualifications

  • 1998 PhD in Biophysics (Photoreactivity of Retinal Pigment Epithelium), Institute of Molecular Biology, Jagiellonian University, Krakow, Poland
  • 1992 MSc in Physics, specialisation in Medical Physics (Photoreactivity of Cationic Derivatives of Porphyrins), Institute of Physics, Jagiellonian University, Krakaow, Poland

Teaching Qualifications

  • 2008 Fellowship of the Higher Education Academy (HEA), UK
  • 2007 Postgraduate Certificate in University Teaching and Learning (PCUTL), Cardiff University

Other Professional Experience

  • 14/01/2013-13/01/2013 sabbatical at the Departments of Ophthalmology and Vision Sciences (Host: Professor Akiko Maeda) and Pharmacology (Host: Professor Krzysztof Palczewski), Case Western Reserve University Medical School, Cleveland, Ohio, USA.
  • 2011-2012 Guest Editor for Symposium-in-Print on Light-Induced Damage to the Retina to be published as a special Issue in Photochemistry and Photobiology
  • 2006-2007 Guest Editor for Symposium-in-Print on Melanins published as a special Issue in Photochemistry and Photobiology
  • since January 2007 Associate Editor for Photochemistry and Photobiology
  • 1993-2000 short term visits (two weeks/year) to Keele University and Paterson Institute for Cancer Research, Christie Hospital NHS Trust, to perform pulse radiolysis experiments in collaboration with Professor T. G.   Truscott and Dr. E. J. Land.
  • 1/07-30/08/1994 research training in Professor Michael A. J.   Rodgers;   laboratory, Dept. of Chemistry, Bowling Green State University, OH, USA; absorption, fluorescence and nanosecond laser flash photolysis study of retinal lipofuscin.
  • 1/10/1993 - 30/09/1997 PhD studies and teaching at the Department of Biophysics, Jagiellonian University; Supervisor: Professor Tadeusz Sarna, PhD
  • 1/10/1992 - 30/09/1993 Research and Teaching Assistant at the Department of Biophysics, Jagiellonian University
  • 1/07-30/08/1991 research training in Professor R Seljelid laboratory, Institute of Medical Biology, Tromso, Norway; 1) comparison of effectiveness of radioprotectants; 2) study of environmental effects on pinocytic activity of phagocytes.

Honours and awards

  • Senior Fulbright Fellowship Identification of the Molecules Responsible for Lipofuscin Phototoxicity in collaboration with Professor J.D. Simon, Duke University, NC, USA, October 2002 - July 2003.
  • Lester Packer Young Investigator Award in appreciation of scientific excellence for presentation of a poster during 2002 World Congress Oxidants and Antioxidants in Biology, a joint meeting of the Oxygen Club of California, Linus Pauling Institute and Society for Free Radical Research International, Santa Barbara, CA, USA, March 2002.
  • Travelling Research Fellowship awarded by the Wellcome Trust, Department of Optometry and Vision Sciences, Cardiff University, Cardiff and School of Chemistry and Physics, Keele University, Keele, UK, July 2000 - July 2002.
  • Award of the Rector of the Jagiellonian University for Excellent PhD Thesis, 1998.
  • Fellowship awarded by the Foundation for Polish Science, 1997.

Professional memberships

  • 2007 - present: Associate Editor for the Photochemistry and Photobiology
  • 2003 - present: Member of the American Society for Photobiology
  • 2005 - Member of the International Carotenoid Society
  • 2001 - present:   Member of the Society for Free Radical Biology and Medicine
  • 1996 - present:   Member of the Association for Research in Vision and Ophthalmology
  • 1995-2010 Member of the European Society for Photobiology

Academic positions

  • Since 1/10/2003 Lecturer, School of Optometry and Vision Sciences, Cardiff University.
  • 15/10/2002-15/07/2003 Visiting Assistant Professor sponsored by Senior Fulbright Fellowship, Department of Chemistry, Duke University, Durham, North Carolina, USA. Host: Professor John D. Simon.
  • 1/10/2000-31/12/2003 Assistant Professor, Department of Biophysics, Faculty of Biotechnology, Jagiellonian University
  • 28/07/2000 - 27/07/2002 Travelling Research Fellowship awarded by the Wellcome Trust, Department of Optometry and Vision Sciences, Cardiff University (Host: Professor Michael E. Boulton) and School of Chemistry and Physics, Keele University (Host: Professor T. George Truscott).
  • 1997 - 2000 Research and Teaching Associate, Department of Biophysics, Institute of Molecular Biology, Jagiellonian University.

Committees and reviewing


Current Postgraduate Students:

Ms. Zahra Raja

Ms. Joy Adomokhai

Past PhD Students:

Dr Linda Bakker

Dr Kinga Handzel

Dr Matthew Davies

Dr Caroline Waters

Dr Carmine Varricchio

Past MSc Students:

Mr. Boyuan Cui

Ms. Sara Heidari

Ms. Syeda Rizvi