L etter to the Editor Lysosomal enzymes activity in patients with pseudoexfoliation syndrome Hanna Lesiewska, 1 Gra _ zyna Malukiewicz, 1 Dorota Olszewska- Slonina 2 and Alina Wozniak 3 1 Department of Ophthalmology, The Nicolaus Copernicus University, Ludwik Rydygier’s Collegium Medicum, Bydgoszcz, Poland; 2 Laboratory of Cell Biology and Genetics, The Nicolaus Copernicus University, Ludwik Rydygier’s Collegium Medicum, Bydgoszcz, Poland; 3 Department of Medical Biology, The Nicolaus Copernicus University, Ludwik Rydygier’s Collegium Medicum, Bydgoszcz, Poland doi: 10.1111/aos.12409 Editor, P seudoexfoliation syndrome (PEX) is a complex systemic disorder of the extracellular matrix affecting the eye and visceral organs. Pseudoexfoli- ation material deposits on various structures of the anterior segment of the eye and around blood vessels of connective tissue. Animal studies have suggested that the lysosomal trafficking regulator (LYST) gene is potentially important in PEX (Liton et al. 2009). Lysosomes are the cellular recycling centres responsible for the physiologic turnover of cell constituents. Inade- quate enzyme activity results in disrup- tion of the degradation process and accumulation of substrates for that specific enzyme, leading to variety of pathological changes. Increasing evidence suggests that the oxidative antioxidative balance is disturbed in patients with PEX (Uc ßakhan et al. 2006; Lesiewska-Junk et al. 2013). The lysosomal proteolytic activity is compromised under oxidative stress conditions (Wenger et al. 2013). We studied 52 consecutive patients with PEX (16 males and 36 females), who presented for senile cataract surgery, median 75 years, range 59 89. The reference group consisted of 30 individuals (10 males and 20 females), matched for age and gender, with senile cataract without PEX, median 72 years, range 6190. Both groups did not differ in stage of cataract nor body mass index and smoking habits. PEX was recognized based on typical material in the anterior segment seen after pupil dilation. The exclusion cri- teria were systemic and local diseases except cataract and PEX (including diabetes, rheumatoid arthritis, lipid profile disorders, intraocular surgery in history). The activity of four lyso- somal enzymes in plasma was assessed as follows: acid phosphatase (AcP) with the use of Bessey method, alpha- 1-antitrypsin (AAT) using Eriksson method, cathepsin D (CAT D) using Anson method and arylsulphatase (AS) using Robinson method. Kolmogorov Smirnov test was used to assess nor- mality of the data. Mann-Whitney test was used for comparison of data from small size independent samples. P- value of <0.05 was considered statisti- cally significant. The values of activities of assessed enzymes are shown in Table 1. Reduced activity of proteolytic enzymes and subtle inflammatory pro- cesses may trigger the PEX-specific fibrotic matrix process (Schl otzer- Schrehardt 2012). Although Mizuno et al. (1980) found acid phosphatase activity significantly higher in the aqueous humour of eyes with PEX than in that of cataractous eyes with- out PEX, in our group, these values in blood plasma appeared to be lower in PEX patients. According to Cumurcu et al. (2008) serum A-1-AT activity was increased in patients with PEX, which is in accordance with our results. It may indicate the role of inflammation in this group of patients. To our best knowledge, this is the first study on AS and CAT D activities in PEX patients. Our observations may shed light on the complex metabolic contribution and molecular pathway of the disease. References Cumurcu T, Ozyurt H Demir HD & Yardim H (2008): Serum alpha-1-antitriypsin levels in patients with pseudoexfolative syndrome. Curr Eye Res 33: 159162. Lesiewska-Junk H, Malukiewicz G, Ols- zewska-Slonina D, Wozniak A & Jung S (2013): Erythrocytes’ oxidative stress markers in patients with pseudoexfoliation syndrome. Acta Ophthalmol 91: e648 e649. Liton PB, Lin Y, Gonzalez P & Epstein DL (2009): Potential role of lysosomal dys- function in the pathogenesis of primary open angle glaucoma. Autophagy 5: 122 124. Mizuno K, Hara S, Ishiguro S & Takei Y (1980): Acid phosphatase in eyes with pseudoexfoliation. Am J Ophthalmol 89: 482489. Schlotzer-Schrehardt U (2012): Neue pathoge- netische Erkenntnisse zum Pseudoexfolia- tions-Syndrom/Glaukom. Ophthalmologe 109: 944951. Uc ßakhan OO, Karel F, Kanpolat A, Devrim E & Durak I (2006): Superoxide dismu- tase activity in the lens capsule of patients with pseudoexfoliation syndrome and cataract. J Cataract Refract Surg 32: 618622. Table 1. Lysosomal enzymes activity in blood plasma Enzyme Median (Q 1 ÀQ 3 ) p PEX Controls AcP 0.924 9 10 À3 nM p-nitrophenol/mg protein/min (Q 1 = 0.821; Q 3 = 1.116) 1.185 9 10 À3 nM p-nitrophenol/mg protein/min (Q 1 = 0.851; Q 3 = 1.392) 0.008 AAT 0.7290 mg inhibited trypsin/ml (Q 1 = 0.6640; Q 3 = 0.8110) 0.5970 mg inhibited trypsin/ml (Q 1 = 0.6603; Q 3 = 0.7690) 0.004 CAT D 15.12 nM released tyrosine/mg protein/min (Q 1 = 13.94; Q 3 = 16.66) 14.82 nM released tyrosine/mg protein/min (Q 1 = 13.62; Q 3 = 16.31) 0.5 AS 1.828 9 10 À3 nM 4NC/mg protein/min (Q 1 = 1.557; Q 3 = 2.138) 1.432 4NC/mg protein/min (Q 1 = 1.022; Q 3 = 1.851) 0.003 AcP = acid phosphatase, AAT = alpha-1-antitrypsin, CAT D = cathepsin D, AS = arylsulpha- tase. 1 Acta Ophthalmologica 2014