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Title: Protection against ethanol-induced osteopenia in female mice by dietary antioxidants

item ALUND, ALEX - Arkansas Children'S Nutrition Research Center (ACNC)
item MERCER, KELLY - Arkansas Children'S Nutrition Research Center (ACNC)
item PULLIAM, C - University Arkansas For Medical Sciences (UAMS)
item SUVA, LARRY - University Arkansas For Medical Sciences (UAMS)
item Badger, Thomas
item RONIS, MARTIN - Arkansas Children'S Nutrition Research Center (ACNC)

Submitted to: Alcoholism: Clinical and Experimental
Publication Type: Abstract Only
Publication Acceptance Date: 3/15/2014
Publication Date: 6/1/2014
Citation: Alund, A.W., Mercer, K.E., Pulliam, C.F., Suva, L.J., Badger, T.M., Ronis, M.J. 2014. Protection against ethanol-induced osteopenia in female mice by dietary antioxidants. Alcoholism: Clinical and Experimental. 38(Supplement s1):Abstract #0103:p. 26A.

Interpretive Summary: In this study we fed mice an 8 week liquid diet with or without alcohol and also with or without one of three dietary antioxidants, Curcumin, N-acetyl cysteine (NAC), and Vitamin E (alpha-tocopherol) to see if regular consumption dietary antioxidants could protect against alcohol induced osteopenia. P-QCT and microCT analysis of tibias showed a protective effect against trabecular bone loss from NAC and Vitamin E, but not from Curcumin consumption. RNA analysis showed that NAC and Vitamin E increase the osteoblastogenic marker, Osteocalcin, and, in the presence of alcohol, decrease the osteoclastogenic marker, TRAP. These findings show a potential protective effect from dietary supplementation with NAC and Vitamin E, but not Curcumin, on alcohol induced trabecular bone loss.

Technical Abstract: Chronic alcohol consumption leads to increased fracture risk and an elevated risk of osteoporosis by decreasing bone mineral density through increasing osteoclast activity and decreasing osteoblast activity. Our lab has shown this mechanism to be mediated by reactive oxygen species (ROS) produced by NADPH oxidases (NOX). It was hypothesized that different dietary antioxidants, Curcumin (120mg/kg/d), N-acetyl cysteine (NAC) (1.2mg/kg/d)), and Vitamin E (alpha-tocopherol) (60mg/kg/d)) would be able to attenuate the NOX produced ROS effects on bone due to chronic alcohol intake. To study the effects of these antioxidants, female mice received a high fat (35%) Lieber DeCarli liquid diet supplemented with an antioxidant with or without EtOH at 30% of total calories for 8 weeks. Ex vivo peripheral-QCT analyses of formalin fixed tibias showed decreased cortical bone mineral density in both the EtOH and EtOH+antioxidant groups compared to pair-fed (PF) and PF+antioxidant groups (P<0.05). However, there was protection from trabecular bone loss in the EtOH+NAC and EtOH+a-tocopherol groups compared to the EtOH group (P<0.05). MicroCT analysis showed a significant decrease in bone volume (BV/TV) and trabecular number (Tb.N) (P<.05), along with a significant increase in trabecular spacing (Tb.Sp) in the EtOH compared to PF (P<.05). In contrast, the EtOH+NAC and EtOH+a-tocopherol did not statistically differ from their respective PF controls. Preliminary femur mRNA analysis showed a significant increase in the osteoblastogenic marker, osteoclacin (OC), in PF+NAC and PF+ alpha-tocopherol compared to PF mice (P<0.05) and no significant effects of EtOH on OC mRNA expression in these groups. In EtOH+NAC and EtOH+alpha-tocopherol groups a decrease in the osteoclastogenic marker, TRAP, was observed compared to the EtOH group (P<0.05). These results suggest a potential protective effect of the dietary antioxidants NAC and alpha-tocopherol at these doses with regard to alcohol effects on bone turnover and trabecular bone loss. In contrast, no significant protective effects were observed following dietary curcumin supplementation.