Macular perfusion changes in people administered two types of COVID-19 vaccines: optical coherence tomography angiography study.

PURPOSE: To evaluate macular chorioretinal flow changes on optical coherence tomography angiography, in participants who received inactivated and messenger RNA (mRNA) vaccines to prevent Coronavirus disease 2019 (COVID-19). METHODS: In this prospective cohort study, healthy participants who received two doses of an inactivated COVID-19 vaccine (CoronaVac) and then one dose of an mRNA vaccine (BNT162b2) were examined before and after each vaccination. Ophthalmologic examination and imaging with optical coherence tomography angiography were performed during each visit. We evaluated vascular densities in the superficial and deep capillary plexuses in foveal, parafoveal, and perifoveal areas; the foveal avascular zone; and choriocapillaris flows (in 1- and 6-mm-diameter areas). RESULTS: One eye in each of the 24 participants was assessed. Superficial capillary plexus vascular densities in the parafoveal area were significantly lower after the second dose of the CoronaVac vaccine than after the first dose. In the deep capillary plexus, vascular attenuation was observed only in the parafoveal region after the first CoronaVac dose. However, in all regions, the deep capillary plexus vascular densities and subfoveal choriocapillaris flow were significantly decreased after the second CoronaVac dose. After the BNT162b2 dose, the superficial capillary plexus vascular densities, the deep capillary plexus vascular densities, and subfoveal choriocapillaris flow of most regions were significantly lower than those before vaccinations. CONCLUSION: Vascular attenuation, observed particularly after the second dose of the CoronaVac vaccine, may explain the pathogenesis of postvaccine ocular ischemic disorders reported in the literature. However, these disorders are extremely rare, and the incidence of thrombotic events caused by COVID-19 itself is higher.

Macular perfusion changes in people administered two types of COVID-19 vaccines: optical coherence tomography angiography study

ABSTRACT Purpose: To evaluate macular chorioretinal flow changes on optical coherence tomography angiography, in participants who received inactivated and messenger RNA (mRNA) vaccines to prevent coronavirus disease 2019 (COVID-19). Methods: In this prospective cohort study, healthy participants who received two doses of an inactivated COVID-19 vaccine (CoronaVac) and then one dose of an mRNA vaccine (BNT162b2) were examined before and after each vaccination. Ophthalmologic examination and imaging with optical coherence tomography angiography were performed during each visit. We evaluated vascular densities in the superficial and deep capillary plexuses in foveal, parafoveal, and perifoveal areas; the foveal avascular zone; and choriocapillaris flows (in 1- and 6-mm-diameter areas). Results: One eye in each of the 24 participants was assessed. Superficial capillary plexus vascular densities in the parafoveal area were significantly lower after the second dose of the CoronaVac vaccine than after the first dose. In the deep capillary plexus, vascular attenuation was observed only in the parafoveal region after the first CoronaVac dose. However, in all regions, the deep capillary plexus vascular densities and subfoveal choriocapillaris flow were significantly decreased after the second CoronaVac dose. After the BNT162b2 dose, the superficial capillary plexus vascular densities, the deep capillary plexus vascular densities, and subfoveal choriocapillaris flow of most regions were significantly lower than those before vaccinations. Conclusion: Vascular attenuation, observed particularly after the second dose of the CoronaVac vaccine, may explain the pathogenesis of postvaccine ocular ischemic disorders reported in the literature. However, these disorders are extremely rare, and the incidence of thrombotic events caused by COVID-19 itself is higher.

Comparison of Endoscopically Assisted Primary Probing and Bicanalicular Silicone Intubation for Congenital Nasolacrimal Duct Obstruction in Children Aged 4 to 7 Years.

PURPOSE: To compare the clinical outcomes of primary nasolacrimal duct probing and primary bicanalicular intubations with endoscopic assistance for congenital nasolacrimal duct obstruction (CNLDO) in children aged 4 to 7 years. METHODS: Forty-three eyes of 43 children (25 boys and 18 girls) with congenital epiphora who underwent primary unilateral probing and bicanalicular intubation were evaluated retrospectively. The tubes were removed 3 to 4 months after their placement, and the children were followed up for another 6 months after their removal. Treatment success was defined as the normal result of the fluorescein dye disappearance test and complete resolution of the lacrimal symptoms and signs of patients. The success rates were compared between the two groups (bicanalicular intubation vs probing). Type of CNLDO (membranous, incomplete complex, and complete complex) was determined with an endonasal endoscope. RESULTS: The mean age was 63.3 ± 11.1 months (range: 48 to 84 months) for the probing group and 64.4 ± 12.1 months (range: 48 to 84 months) for the bicanalicular intubation group (P = .915). The bicanalicular intubation group showed significantly greater treatment success (21 of 24, 87.5%) compared to the probing group (11 of 19, 57.9%; P = .038). Bicanalicular intubation provided higher treatment success among patients with complex CNLDO compared to probing (80.0% vs 11.1%, P = .002). There was no difference in mean age between the patients with successful and failed treatment in both groups (P = .631 and .137, respectively). CONCLUSIONS: Bicanalicular intubation was associated with a higher success rate than probing under nasal endoscopic visualization for the treatment of CNLDO in children aged 4 to 7 years. The type of CNLDO might be the primary factor for the treatment success. [J Pediatr Ophthalmol Strabismus. 2023;60(2):101-107.].

Ameliorative Effects of Testosterone Administration on Renal Redox Homeostasis in Naturally Aged Rats.

BACKGROUND: Testosterone biosynthesis gradually decreases with age. Impaired redox homeostasis-related oxidative damage in cellular macromolecules has a high risk for the development of renal insufficiency. Our aim was to study the effects of testosterone replacement therapy on redox homeostasis. METHODS: We investigated various oxidative damage biomarkers in kidney. Experimental animals were separated into three groups-naturally aged rats, testosterone-administered naturally aged rats (single dose of 25 mg/kg testosterone enanthate), and their respective young controls. RESULTS: Our results showed that the testosterone-administered naturally aged group shared significant similarities with the young rats with respect to their redox status. In testosterone-administered naturally aged rats, kynurenine, protein carbonyl, advanced oxidation protein products, lipid peroxidation markers, and xanthine oxidase activities were significantly lower and Cu-Zn superoxide dismutase activities and testosterone levels were higher than naturally aged rats. In testosterone-administered naturally aged rats, catalase activities, ferric reducing anti-oxidant power, and testosterone levels were significantly lower and dityrosine, N-formyl kynurenine, protein carbonyl, and protein hydroperoxides were significantly higher than in young rats. On the other hand, in naturally aged rats, Cu-Zn superoxide dismutase, catalase activities, ferric reducing anti-oxidant power, and testosterone levels were lower and dityrosine, kynurenine, protein carbonyl, protein hydroperoxide, advanced oxidation protein products, lipid peroxidation markers, advanced glycation end products, and xanthine oxidase activities were higher than controls. CONCLUSIONS: Our results showed that a single dose of testosterone administration has a positive effect on the redox status of the aged kidney. Future studies are needed to clarify the exact molecular mechanism(s) involved in the action of testosterone in maintaining kidney redox homeostasis.

Age-related changes in rat prostate tissue; perspective of protein oxidation.

BACKGROUND: Increased systemic oxidative stress is considered as an important risk factor for prostate cancer occurrence; however, the relationship between impaired redox homeostasis of prostate tissue and aging remains unclear. OBJECTIVE: In our study, we hypothesized that age-related deterioration of redox homeostasis in prostate tissue may be considered as a predisposing factor for prostate cancer occurrence. METHODS: Sprague-Dawley rats were divided into two groups as young control (5 months) and naturally aged (24 months). We investigated the levels of oxidant and antioxidant parameters in prostate tissue. RESULTS: Advanced oxidation protein products, protein carbonyl, non-protein thiol and lipid hydroperoxides levels of aged rats were significantly higher than in the young control rats (p < 0.01, p < 0.05, p < 0.001, p < 0.05, respectively). Additionally, antioxidant activity of Cu-Zn-superoxide dismutase in elderly group was significantly lower than young controls (p < 0.05). CONCLUSIONS: We suggest that increased non-protein thiol levels found in aged rats may prevent further dissemination of oxidative protein damage. We also propose that the increased levels of oxidative protein damage markers and decreased Cu-Zn superoxide dismutase activity in aged prostate may be considered as a predisposing factor for prostate cancer. Further studies are warranted to clarify all these oxidative changes as initiation factors for prostate cancer in the association of aging with prostate cancer.

A comprehensive study of myocardial redox homeostasis in naturally and mimetically aged rats.

Age-related myocardial dysfunction has important implications with impaired redox homeostasis. Current study focused on investigation of redox homeostasis and histopathological changes in the myocardium of mimetically (MA), naturally aged (NA), and young control (YC) rats. Chronic D-galactose administration to young male Wistar rats (5 months old) was used to set up experimental aging models. We investigated 16 different oxidative damage biomarkers which have evaluated redox homeostasis of cellular macromolecules such as protein, lipid, and DNA. As a protein oxidation biomarker, advanced oxidation end products, protein carbonyl groups, protein-bound advanced glycation end products, dityrosine, kynurenine, and N-formylkynurenine concentrations in MA and NA rats were found to be significantly higher compared to those in YC rats. On the other hand, the levels of protein thiol groups were not significantly different between groups, whereas lipid peroxidation biomarkers such as conjugated diens, lipid hydroperoxides, and malondialdehyde in MA and NA rats were found to be significantly higher in comparison to those in YCs. For the assessment of oxidative DNA damage, we analyzed eight hydroxy-5'-deoxyguanosine concentrations of MA and NA groups which were higher than YCs. As an antioxidant status in the MA and NA groups, Cu-Zn superoxide dismutase, ferric reducing antioxidant power, and total thiol levels were lower than those in the YCs. Only nonprotein thiol levels were not significantly different. We also observed similar histopathological changes in MA and NA rats. We concluded that the mimetic aging model could be considered as a reliable experimental model for myocardial senescence.

Oxidation scrutiny in persuaded aging and chronological aging at systemic redox homeostasis level.

BACKGROUND: The effect of the natural aging process on systemic redox homeostasis is previously documented. However, none of the studies specify the effect of experimental aging on systemic redox homeostasis. The purpose of this study is to clarify the ambiguity raised in preliminary reports as to mimetic aging dependency of the type and magnitude of oxidative damage on constituents of plasma. METHODS: In the current study, we investigated the interrelationship among various groups of the systemic oxidative damage markers such as protein oxidation products (protein carbonyl groups, protein hydroperoxides, advanced oxidation protein products, protein thiol groups), lipid peroxidation products (malondialdehyde, lipid hydroperoxides, conjugated dienes), glycoxidation adducts (advanced glycation end products), and antioxidant capacity (ferric reducing/antioxidant power, Cu,Zn-superoxide dismutase, total thiol, non-protein thiol). All these markers were measured in plasma of mimetically aged (MA) rats (5-month-old rats subjected to d-galactose-induced experimental aging), naturally aged (NA) rats (24-month-old), and their corresponding young controls (YC) (5months old). RESULTS AND CONCLUSIONS: Our current results show that systemic oxidation markers of the MA group share significant similarities in terms of impaired redox homeostasis with the NA rats and may be considered as a reliable experimental aging model for intravascular aging. Additional methodological studies including d-galactose dosage and application time are warranted to clarify the potential involvement of all these systemic redox variations as mechanistic factors in the development of mimetic aging related intravascular deterioration. Reversing or preventing systemic oxidative damage in experimental and natural aging should therefore be considered the primary target for the development of effective therapeutic strategies to prevent or treat age-related vascular disorders.