Effects of short-term exposure to low doses of bisphenol A on cellular senescence in the adult rat kidney.

Publisher: Springer Country of Publication: Germany NLM ID: 9506663 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1432-119X (Electronic) Linking ISSN: 09486143 NLM ISO Abbreviation: Histochem Cell Biol Subsets: MEDLINE

Original Publication: Berlin : Springer,

Lipofuscin* ; Cellular Senescence*; Rats ; Animals ; Male ; Rats, Wistar ; Kidney

Bisphenol A (BPA) is one of the primary chemicals produced by volume worldwide. Extensive literature has raised many concerns about its possible involvement in the pathogenesis of kidney diseases, but its contribution has not been extensively studied. During cellular senescence, the interference of lipofuscin with cellular functions promotes further senescence, causing cellular malfunction. Insulin-like growth factor-1 (IGF-1) plays an important protective role in the setting of kidney injury. The goal of the present work was to evaluate the effects of short-term treatment with low doses of BPA on cellular senescence in adult rat kidneys. Male Wistar rats were injected with vehicle (CONTROL group) or 50 or 500 μg/kg/day of BPA for 1 week (BPA50 and BPA500 groups, respectively). The kidneys were fixed in 4% buffered formaldehyde and embedded in paraffin. Immunohistochemical analyses were performed, and an immunoreactive score (IRS) was calculated. Lipofuscin autofluorescence was used for the study of cellular senescence. The renal cortex showed diffuse autofluorescent lipofuscin signal in the proximal convoluted tubules (PCTs) of males in the BPA50-treated (weak intensity) and BPA500-treated (strong intensity) groups, but not in CONTROL males. Labeling of cortical PCTs with anti-IGF-1 antibodies showed an IRS of 0 in the CONTROL group, but IRSs of 4 and 6 in the BPA50- and BPA500-treated groups, respectively. The present results suggest that low, "safe" doses of BPA induce renal injury, as measured by histological signs of renal changes, increased cellular senescence, and activation of cellular repair systems in PCTs.
(© 2023. The Author(s).)

PLoS One. 2015 Apr 30;10(4):e0126029. (PMID: 25927440)
J Cell Biol. 2011 Feb 21;192(4):547-56. (PMID: 21321098)
Cell. 2013 Jun 6;153(6):1194-217. (PMID: 23746838)
J Am Soc Nephrol. 1994 Jul;5(1):1-11. (PMID: 7948775)
Front Pharmacol. 2020 May 26;11:755. (PMID: 32528288)
Kidney Int. 2001 Feb;59(2):725-31. (PMID: 11168955)
Bioanalysis. 2016 Jun;8(11):1145-58. (PMID: 27217162)
Curr Opin Crit Care. 2005 Dec;11(6):555-65. (PMID: 16292059)
Biomolecules. 2021 Apr 29;11(5):. (PMID: 33946939)
Toxicol Rep. 2022 Mar 22;9:521-533. (PMID: 35371924)
Int Rev Cytol. 1981;73:149-82. (PMID: 7028659)
Pathologe. 1987 May;8(3):138-40. (PMID: 3303008)
Kidney Int. 2011 Jul;80(1):29-40. (PMID: 21562469)
Redox Rep. 2001;6(1):15-26. (PMID: 11333111)
Int J Clin Exp Pathol. 2012;5(3):187-94. (PMID: 22558472)
J Cell Mol Med. 2004 Oct-Dec;8(4):474-87. (PMID: 15601576)
J Cell Physiol. 2014 Dec;229(12):2057-66. (PMID: 24809654)
J Am Soc Nephrol. 2018 Apr;29(4):1238-1256. (PMID: 29440280)
Mol Cell Endocrinol. 2022 Jan 1;539:111415. (PMID: 34339825)
Mol Pathol. 2001 Jun;54(3):133-7. (PMID: 11376123)
Food Chem Toxicol. 2018 Apr;114:270-277. (PMID: 29477810)
Toxicol Appl Pharmacol. 2010 Oct 1;248(1):1-11. (PMID: 20655935)
Int J Environ Res Public Health. 2022 Oct 26;19(21):. (PMID: 36360773)
Front Med (Lausanne). 2021 Oct 15;8:745803. (PMID: 34722583)
Biomolecules. 2021 Jul 16;11(7):. (PMID: 34356670)
Eur J Histochem. 2015 Feb 06;59(1):2485. (PMID: 25820564)
Environ Health Perspect. 2011 Apr;119(4):422-30. (PMID: 20855240)
Toxicol Pathol. 2012 Jun;40(4 Suppl):14S-86S. (PMID: 22637735)
Mech Ageing Dev. 1998 Sep 1;104(3):277-91. (PMID: 9818731)
Crit Care Clin. 2005 Apr;21(2):197-210. (PMID: 15781157)
Mol Cell Biol. 1999 Oct;19(10):7203-15. (PMID: 10490655)
Arch Pathol Lab Med. 1985 Aug;109(8):716-21. (PMID: 3893381)
Aging Cell. 2020 Dec;19(12):e13270. (PMID: 33166065)
Aging (Albany NY). 2013 Jan;5(1):37-50. (PMID: 23449538)
Kidney Int. 2004 Feb;65(2):510-20. (PMID: 14717921)
Environ Health. 2015 Feb 11;14:13. (PMID: 25971433)
Int J Mol Sci. 2021 Jul 03;22(13):. (PMID: 34281243)
J Dev Orig Health Dis. 2015 Dec;6(6):520-9. (PMID: 26234469)
Kidney Int. 2012 Jul;82(2):172-83. (PMID: 22437410)
J Am Soc Nephrol. 2010 Sep;21(9):1436-9. (PMID: 20705707)
Front Endocrinol (Lausanne). 2018 Apr 09;9:117. (PMID: 29686648)
Nefrologia. 2010;30(4):385-93. (PMID: 20651879)

PAPI-20-PUENTE-12; PAPI-19-PUENTE-15. Grants from the University of Oviedo

Keywords: Aging; Biomarker; Endocrine disruption; IGF-1; Kidney; Lipofuscin

MLT3645I99 (bisphenol A)
0 (Lipofuscin)

Date Created: 20230109 Date Completed: 20230519 Latest Revision: 20230520

20231215

PMC10192151

10.1007/s00418-022-02178-x

36622388