Cell deletion by apoptosis during regression of rat parotid sialadenosis.
Enlargement of the rat parotid salivary glands was induced by repeated administration of isoproterenol. Mean wet weights of the treated glands increased steadily to 240% of control values. Following withdrawal of the drug, quantitative histological techniques were used to investigate the balance between hypertrophy, hyperplasia and apoptosis. The volume occupied by acinar cells relative to the total gland volume together with cytoplasmic magnitude of nuclear area ratios as measures of hypertrophy increased during the early experimental period. Similarly, serous acinar cell mitotic counts increased, indicating that hyperplasia had occurred. Apoptosis was demonstrated at light microscopical level to be the main mechanism for cell deletion as the glands returned to normal size and weight. The results indicate that hypertrophy and hyperplasia of serous acinar cells contribute to isoproterenol-induced sialadenosis. The experimental animal model demonstrates that these proliferative changes are completed by 48 h and thereafter are balanced by apoptosis as the glands recover their normal size and weight.
Chisholm
D M
DM
Department of Dental Surgery and Periodontology, University of Dundee, Dental Hospital and School, Scotland.
Adi
M M
MM
Ervine
I M
IM
Ogden
G R
GR
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D004195:Disease Models, Animal; D007545:Isoproterenol; D008297:Male; D008940:Mitotic Index; D009929:Organ Size; D010305:Parotid Diseases / Q000139:chemically induced / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D012074:Remission Induction; D013997:Time Factors
D007545:Isoproterenol