Aziz Rodan Sarohan

Dr. Aziz Rodan Sarohan

orcid

Research Focus & Metrics

Academic Career Length

7Years (2020-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 November 2020 in Medical Hypotheses
Verified
Journal Article
Closed access
ASAziz Rodan Sarohan
Aziz Rodan Sarohan

23 August 2021 in Cellular Signalling
Verified
Journal Article
Closed access
ASAziz Rodan Sarohan
Aziz Rodan Sarohan
MKMurat Kızıl
Murat Kızıl
AIAhmet Çağkan İnKaya
Ahmet Çağkan İnKaya
SMShokhan Mahmud
Shokhan Mahmud
MAMuhammad Akram
Muhammad Akram
OCOsman Cen
Osman Cen

28 May 2022 in Clinical Nutrition Open Science
Verified
Journal Article
Open access
ASAziz Rodan Sarohan
Aziz Rodan Sarohan
HAHakan Akelma
Hakan Akelma
EAEşref Araç
Eşref Araç
ÖAÖzgür Aslan
Özgür Aslan
OCOsman Cen
Osman Cen
COVID-19 has been a devastating pandemic. There are indications that vitamin A is depleted during infections. Vitamin A is important in development and immune homeostasis. It has been used successfully in measles, RSV and AIDS infections. In this study, we aimed to measure the serum retinol levels in severe COVID-19 patients to assess the importance of vitamin A in the COVID-19 pathogenesis. The serum retinol level was measured in two groups of patients: the COVID-19 group, which consisted of 27 severe COVID-19 patients hospitalized in the intensive care unit with respiratory failure, and the control group, which consisted of 23 patients without COVID-19 symptoms. The mean serum retinol levels were 0.37 mg/L in the COVID-19 group and 0.52 mg/L in the control group. The difference between the serum retinol levels in the two groups was statistically significant. There was no significant difference in retinol levels between different ages and genders within the COVID-19 group. Comorbidity did not affect serum retinol levels. The serum retinol level was significantly lower in patients with severe COVID-19, and this difference was independent of age or underlying comorbidity. Our data show that retinol and retinoic acid signaling might be important in immunopathogenesis of COVID-19.

1 February 2021 in medRxiv
Verified
Preprint
Open access
PDF file
ASAziz Rodan Sarohan
Aziz Rodan Sarohan
HAHakan Akelma
Hakan Akelma
EAEşref Araç
Eşref Araç
ÖAÖzgür Aslan
Özgür Aslan
Background and Purpose Vitamin A is depleted during infections. Vitamin A has been used successfully in measles, RSV and AIDS patients and is an effective vaccine adjuvant. In this study, low retinol levels were found in patients with severe COVID-19. Retinoid signaling impairment in COVID-19 disrupts Type-I interferon synthesis. Material and Method Two groups were formed in the study. The patient group consisted of 27 (Group 1) severe COVID-19 patients hospitalized in the intensive care unit with respiratory failure, and the control group consisted of 23 (Group 2) patients without COVID-19 symptoms. Serum retinol levels were analyzed by ELIZA and HPLC in both groups. Findings Retinol levels were found to be significantly lower in the patient group (P 0.05). There was no significant difference in retinol between men and women (P> 0.05). Comorbidity did not affect serum retinol levels (P >0.05). Conclusion Serum retinol levels were low in patients with severe COVID-19. Drugs preventing retinol excretion were not stopped in the patient group. Some patients took vitamin A externally. Despite this, retinol was low in COVID-19 patients. Retinol depletion impairs Type-I interferon synthesis by impairing retinoid signaling. Retinoid signaling may be the main pathogenetic disorder in COVID-19. This pathogenesis can serve as a guide for adjuvants, drug targets, and candidate drugs. Retinol, retinoic acid derivatives, and some CYP450 inhibitors may work on COVID-19.


6 April 2022 in SciELO Preprints
Verified
Preprint
Open access
ASAziz Rodan Sarohan
Aziz Rodan Sarohan
ATAlpay Tuncar
Alpay Tuncar
ASAbdurrahman Sarohan
Abdurrahman Sarohan
The paper has been withdrawn owing to identification of uncited similarities with other text(s).