300
AUGUST EPPLE
canicula, Raja asterias, and Torpedo marmorata. However, he also observed lesions in the exocrine pancreas, as well as in the interrenal organ,
adrenal bodies, and kidney tubules. Clausen (1953) reports B-cell destruction in two specimen of Scyliorhinus canicula after subcutaneous
injection of relatively low doses of alloxan; the A cells of these animals
appeared hypertrophied as in sharks, as reported by Saviano (1947a). In
Hydrolagus colZiei, Patent (1968) describes selective damage of the B
cells after injection of only 300 mg/kg body weight into the cannulated
dorsal aorta.
It appears difficult to explain the differences between these findings.
Perhaps the manner of injection is of paramount importance in chondrichthyans since alloxan may be immediately inactivated by the abundance of urea, forming alluranic acid (Kern, 1966). However, the urea
content in the blood of the holocephalians is at least as high as that of the
selachians (see chapter by Forster and Goldstein, Volume I). Thus, the
results of Patent (1968) show that urea is not responsible for the
difference.
Many studies deal with the diabetogenic action of alloxan in teleosts
(Saviano, 1947b; Lazarow and Berman, 1947; Doerr, 1950; La Grutta,
1950; Grosso, 1950; Mosca, 1959; Clausen, 1953; Schatzle, 1954; Nace,
1955, 1960; Murell and Nace, 1959; Nace et al., 1958, 1959; J. Davidson,
1959; Ghiani and Federici, 1960; Falkmer, 1961; Falkmer and Olsson,
1962; Moule and Nace, 1963; Young and Chavin, 1963,1966; Khanna and
Mehrotra, 1969). Several investigators describe B-cell lesions following
alloxan injection, the degree of these lesions varying greatly. For example,
Doerr (1950) concludes that a specific alloxan diabetes cannot be produced in Cyprinidae; on the other hand, Falkmer ( 1961) finds hyperglycemia and B-cell destruction for as long as 3 weeks after alloxan treatment in Cottus scorpius. The morphology of B-cell destruction in teleosts
is well documented in the publications of Murrel and Nace (1959) and
Falkmer ( 1961). Matty and Qureshi ( 1967) observed in alloxan-treated
islets of Cottus a decline of the RNA content. Since several investigators
found destruction of other tissues such as liver, kidney, and exocrine pancreas (Saviano, 194%; Doerr, 1950; Grosso, 1950; Mosca, 1959; Schatzle,
1954; Murell and Nace, 1959; Falkmer, 1961; Young and Chavin, 1966),
suitable histological controls are necessary to determine whether the
hyperglycemia, after alloxan injection, results from selective B-cell destruction or the toxic effects on other organs. Also, the question arises as to
whether the term “alloxan diabetes” is justified. Hyperglycemia without
concomitant impairment of the lipid metabolism would not correspond
to the diabetic syndrome in mammals. La Grutta (1950), however, reported hepatic steatosis in alloxan-treated specimens of Scorpaenu scrofa.
Since this could be prevented by insulin application, it suggests that the
AUGUST EPPLE
canicula, Raja asterias, and Torpedo marmorata. However, he also observed lesions in the exocrine pancreas, as well as in the interrenal organ,
adrenal bodies, and kidney tubules. Clausen (1953) reports B-cell destruction in two specimen of Scyliorhinus canicula after subcutaneous
injection of relatively low doses of alloxan; the A cells of these animals
appeared hypertrophied as in sharks, as reported by Saviano (1947a). In
Hydrolagus colZiei, Patent (1968) describes selective damage of the B
cells after injection of only 300 mg/kg body weight into the cannulated
dorsal aorta.
It appears difficult to explain the differences between these findings.
Perhaps the manner of injection is of paramount importance in chondrichthyans since alloxan may be immediately inactivated by the abundance of urea, forming alluranic acid (Kern, 1966). However, the urea
content in the blood of the holocephalians is at least as high as that of the
selachians (see chapter by Forster and Goldstein, Volume I). Thus, the
results of Patent (1968) show that urea is not responsible for the
difference.
Many studies deal with the diabetogenic action of alloxan in teleosts
(Saviano, 1947b; Lazarow and Berman, 1947; Doerr, 1950; La Grutta,
1950; Grosso, 1950; Mosca, 1959; Clausen, 1953; Schatzle, 1954; Nace,
1955, 1960; Murell and Nace, 1959; Nace et al., 1958, 1959; J. Davidson,
1959; Ghiani and Federici, 1960; Falkmer, 1961; Falkmer and Olsson,
1962; Moule and Nace, 1963; Young and Chavin, 1963,1966; Khanna and
Mehrotra, 1969). Several investigators describe B-cell lesions following
alloxan injection, the degree of these lesions varying greatly. For example,
Doerr (1950) concludes that a specific alloxan diabetes cannot be produced in Cyprinidae; on the other hand, Falkmer ( 1961) finds hyperglycemia and B-cell destruction for as long as 3 weeks after alloxan treatment in Cottus scorpius. The morphology of B-cell destruction in teleosts
is well documented in the publications of Murrel and Nace (1959) and
Falkmer ( 1961). Matty and Qureshi ( 1967) observed in alloxan-treated
islets of Cottus a decline of the RNA content. Since several investigators
found destruction of other tissues such as liver, kidney, and exocrine pancreas (Saviano, 194%; Doerr, 1950; Grosso, 1950; Mosca, 1959; Schatzle,
1954; Murell and Nace, 1959; Falkmer, 1961; Young and Chavin, 1966),
suitable histological controls are necessary to determine whether the
hyperglycemia, after alloxan injection, results from selective B-cell destruction or the toxic effects on other organs. Also, the question arises as to
whether the term “alloxan diabetes” is justified. Hyperglycemia without
concomitant impairment of the lipid metabolism would not correspond
to the diabetic syndrome in mammals. La Grutta (1950), however, reported hepatic steatosis in alloxan-treated specimens of Scorpaenu scrofa.
Since this could be prevented by insulin application, it suggests that the