TY - JOUR
T1 - Effect of sodium selenite upon bromobenzene toxicity in rats. I. Hepatotoxicity
AU - Merrick, B. Alex
AU - Davies, Marc H.
AU - Hasegawa, Royhei
AU - St. John, Margaret K.
AU - Cohen, Samuel M.
AU - Schnell, R. Craig
N1 - Funding Information:
Support for this work was provided by NIEHS Research Grant ES-02425, a Blanch Widaman Fellowship (B.A.M.), and a Burroughs-Wellcome Toxicology Scholar Award (R.C.S.).
PY - 1986/4
Y1 - 1986/4
N2 - The effects of sodium selenite on bromobenzene hepatotoxicity were examined in male rats. Rats pretreated with sodium selenite (12.5 or 30 μmol/kg, ip) 72 hr prior to injection of bromobenzene (7.5 mmol/kg, ip) showed a marked reduction in bromobenzene-induced liver injury as evidenced by decreased plasma alanine and aspartate transaminase values, sorbitol dehydrogenase activity, and reduced histologic damage. Administration of bromobenzene did not affect the selenium content of blood or liver. At 72 hr after treatment with selenite, hepatic reduced (GSH) and oxidized (GSSG) glutathione values or GSH synthetic and degradation enzyme activities were not altered. However, from 3 to 12 hr following bromobenzene administration, hepatic GSH and cysteine amounts declined less rapidly in selenite-treated rats compared to control. Thus, acute selenite treatment ameliorated bromobenzene hepatotoxicity in a manner suggesting facilitation of hepatic GSH production by selenite for use in bromobenzene detoxication.
AB - The effects of sodium selenite on bromobenzene hepatotoxicity were examined in male rats. Rats pretreated with sodium selenite (12.5 or 30 μmol/kg, ip) 72 hr prior to injection of bromobenzene (7.5 mmol/kg, ip) showed a marked reduction in bromobenzene-induced liver injury as evidenced by decreased plasma alanine and aspartate transaminase values, sorbitol dehydrogenase activity, and reduced histologic damage. Administration of bromobenzene did not affect the selenium content of blood or liver. At 72 hr after treatment with selenite, hepatic reduced (GSH) and oxidized (GSSG) glutathione values or GSH synthetic and degradation enzyme activities were not altered. However, from 3 to 12 hr following bromobenzene administration, hepatic GSH and cysteine amounts declined less rapidly in selenite-treated rats compared to control. Thus, acute selenite treatment ameliorated bromobenzene hepatotoxicity in a manner suggesting facilitation of hepatic GSH production by selenite for use in bromobenzene detoxication.
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U2 - 10.1016/0041-008X(86)90304-2
DO - 10.1016/0041-008X(86)90304-2
M3 - Article
C2 - 3961815
AN - SCOPUS:0022479666
SN - 0041-008X
VL - 83
SP - 271
EP - 278
JO - Toxicology and Applied Pharmacology
JF - Toxicology and Applied Pharmacology
IS - 2
ER -