Premium
Ultrastructural Injury and Regeneration in the Goldfish Nephron following Sublethal Exposure to Hexachlorobutadiene
Author(s) -
Reimschuessel Renate,
Bennett Richard O.,
May Eric B.,
Lipsky Michael M.
Publication year - 1991
Publication title -
journal of aquatic animal health
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.507
H-Index - 52
eISSN - 1548-8667
pISSN - 0899-7659
DOI - 10.1577/1548-8667(1991)003<0001:uiarit>2.3.co;2
Subject(s) - biology , aminooxyacetic acid , ultrastructure , mitochondrion , nephron , toxicity , nephrotoxicity , epithelium , microbiology and biotechnology , organoid , kidney , anatomy , biochemistry , medicine , endocrinology , enzyme , genetics
The ultrastructure of the damaged and regenerating renal epithelium of goldfish Carassius auratus exposed to hexachlorobutadiene (HCBD) was examined. As in mammals, the target organelles for HCBD‐induced nephrotoxicity are the mitochondria. Extensively swollen mitochondria appeared in proximal segments P2 and P3 within 12 h of HCBD exposure. By 1 week, swollen mitochondria were also present in P 1 epithelial cells. Initially, regenerating epithelial cells in the injured nephrons appeared insensitive to the toxicity. Once they developed more differentiated characteristics, they also developed swollen mitochondria. Newly formed developing nephrons appeared several weeks following toxicant exposure. These also appeared resistant to the toxicity until they became more differentiated. The inhibitor aminooxyacetic acid protected the epithelium from the toxicity, indicating a possible role for cysteine‐conjugate β‐lyase in the bioactivation of HCBD metabolites in the goldfish.