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Background/aims: Arterial stenosis activates the renin-angiotensin-aldosterone system subsequently resulting in renovascular hypertension (RVHT) and renal oxidative injury. We explored the effect of sodium thiosulfate (STS, Na2S2O3), a developed antioxidant in clinical trial, on RVHT-induced hypertension and renal oxidative injury in rats., Methods: We induced RVHT in male Wistar rats with bilaterally partial ligation of renal arteries in the 2-kidney 2-clip model. We evaluated the STS effect on RVHT-induced oxidative injury and apoptosis by a chemiluminescence amplification method, Western blot, and immunohistochemistry., Results: We found STS displayed a dose-dependent antioxidant H2O2 activity and adapted the maximal scavenging H2O2 activity of STS at the dosage of 0.1 g/kg intraperitoneally 3 times/week for 4 weeks in RVHT rats. RVHT induced a significant elevation of arterial blood pressure, blood reactive oxygen species amount, neutrophil infiltration, 4-HNE and NADPH oxidase gp91 expression, Bax/Bcl-2/poly(ADP-ribose) polymerase (PARP)-mediated apoptosis formation, blue Masson-stained fibrosis, and urinary protein level. STS treatment significantly reduced hypertension, oxidative stress, neutrophil infiltration, fibrosis, and Bax/Bcl-2/PARP-mediated apoptosis formation and depressed the urinary protein level in the RVHT models., Conclusion: Our results suggest that STS treatment could ameliorate RVHT hypertension and renal oxidative injury through antioxidant, antifibrotic, and antiapoptotic mechanisms., (© 2020 The Author(s). Published by S. Karger AG, Basel.)

The present study was carried out to determine the conversion factor of synthetic (2)H-labelled beta-carotene to vitamin A in Chinese adults by using a stable-isotope dilution technique. Fifteen healthy volunteers aged 50-60 years were recruited for a 55 d experiment. The volunteers (nine males and six females) were each given a physiological dose of [(2)H8]beta-carotene (6 mg) in oil on the first day of the experiment, and a reference dose of [(2)H8]retinyl acetate (3 mg) in oil was given on the fourth day. Serum samples were collected at 0, 3, 5, 7, 9, 11, and 13 h on the first and the fourth days of the study, daily for 10 d, and then weekly from days 14 to 56. beta-Carotene and retinol were extracted from serum and isolated by HPLC, and their enrichments were respectively determined by using GC-electron capture negative chemical ionisation-MS and LC-atmospheric pressure chemical ionisation interface-MS. Four of the subjects exhibited beta-carotene to vitamin A conversion factors of >29.0:1 on a molar basis and were termed 'poor converters'. In the eleven normal converters (seven males and four females), the calculated conversion factors of beta-carotene to retinol ranged from 2.0:1 to 12.2:1 with an average of 4.8 (sd 2.8):1 on a molar basis, and from 3.8:1 to 22.8:1 with an average of 9.1 (sd 5.3):1 on a weight basis. The 52 d post-intestinal absorption conversion was estimated to be about 30 % of the total converted retinol.

Background/Aims: Arterial stenosis activates the renin-angiotensin-aldosterone system subsequently resulting in renovascular hypertension (RVHT) and renal oxidative injury. We explored the effect of sodium thiosulfate (STS, Na2S2O3), a developed antioxidant in clinical trial, on RVHT-induced hypertension and renal oxidative injury in rats. Methods: We induced RVHT in male Wistar rats with bilaterally partial ligation of renal arteries in the 2-kidney 2-clip model. We evaluated the STS effect on RVHT-induced oxidative injury and apoptosis by a chemiluminescence amplification method, Western blot, and immunohistochemistry. Results: We found STS displayed a dose-dependent antioxidant H2O2 activity and adapted the maximal scavenging H2O2 activity of STS at the dosage of 0.1 g/kg intraperitoneally 3 times/week for 4 weeks in RVHT rats. RVHT induced a significant elevation of arterial blood pressure, blood reactive oxygen species amount, neutrophil infiltration, 4-HNE and NADPH oxidase gp91 expression, Bax/Bcl-2/poly(ADP-ribose) polymerase (PARP)-mediated apoptosis formation, blue Masson-stained fibrosis, and urinary protein level. STS treatment significantly reduced hypertension, oxidative stress, neutrophil infiltration, fibrosis, and Bax/Bcl-2/PARP-mediated apoptosis formation and depressed the urinary protein level in the RVHT models. Conclusion: Our results suggest that STS treatment could ameliorate RVHT hypertension and renal oxidative injury through antioxidant, antifibrotic, and antiapoptotic mechanisms.