Prophylactic Effects of DL-β Hydroxybutyrate against Hepatic Cellular Senescence Induced by D-galactose or γ-irradiation via Partial Modulation of Antioxidants and Trace Elements in Male Rats

Document Type : Original Article


1 Drug Radiation Research Department, National Centre for Radiation Research and Technology (NCRRT), Atomic Energy Authority, P.O. Box; 29 Nasr city, Cairo, Egypt

2 Biochemistry Division, Chemistry Department, Faculty of Science, Tanta University, Tanta, Egypt


Background: aging of cells is a normal feature but, it is important to delay this process and improve the life style. Aim: this work aimed to investigate the possible potential inhibitory effect of DL-β-hydroxybutyrate (βOHB) against hepatic cellular senescence induced by D-galactose or γ-irradiation in rats based on antioxidant and certain trace elements estimation in the liver.  Methods: Six groups of male rats were used as the control, irradiated group (acute dose 5 Gy, 2 weeks), D-galactose (150 mg/kg b.wt, 6 weeks), βOHB (72.8 mg/kg b.wt, 14 days), γ-irradiation plus βOHB, and D-galactose plus βOHB. Results: neither βOHB nor D-galactose administration had a significant effect relative to the normal control value on Hb, MCV, and RBC’s. βOHB along with D-galactose or γ-irradiation significantly increased G6PD activity compared with control group. In D-galactose, or γ-irradiation groups, liver MDA levels and SOD activity were significantly increased. Meanwhile, NO and GSH levels were significantly increased in the γ-irradiation group relative to normal control levels.  The findings showed that βOHB alleviated hematological, antioxidant alterations and modulated the change in Cu, Fe, and Zn elements in D-galactose or γ-irradiation group. The results concur well with histological alteration in our previous findings. Conclusion: these findings highlight a role for βOHB as a potent protective agent against hepatic cellular senescence associated liver injury through enhancing RBC’s G6PD activity, reduction of oxidative stress and partial modulation of trace elements.