The bottom dwelling air-breathing catfish,
Clarias batrachus
(Linn.) also respires via its skin (an
accessory water-breathing organ). Prolonged (90 days) exposure to disodium arsenate heptahydrate has
caused massive damage (e.g. wear and tear of various cellular components including club cells,
hypertrophy and hyperplasia of the goblet mucous cells, altered staining and the slimy secretion) to the
epidermis of its skin. The present study investigated the recovery in architecture of the damaged
epidermis following return of the 90 days disodium arsenate heptahydrate exposed fish to clean water.
The significant regeneration of its different cellular components (epithelial cells, Club cells, Mucous
cells) took place after 24 h of withdrawal when sloughing; wear and tear and other damages of the
epidermis of the skin got substantially reduced. The histopathological alterations which still continued
included squeezing out of contents of the Club cells that formed a thin layer on the body surface.
Regeneration of the Club cells continued throughout the epidermis even though the newly formed Club
cells still showed massive sign of degeneration. Altered staining behaviour and hyperactivity of the
Mucous cells continues even after prolonged withdrawal of the stress of the arsenic salt. Similarly the
glycoproteins of the slime secreted by the mucous cells retained their sulphate moieties. This indicates
that disodium arsenate heptahydrate induces certain permanent non-reversible damages including altered
mucogenic activity in the epidermis of the skin of
C. batrachus.
