A unique property of Drosophila melanogaster l(1)ts403 strain with the defect in heat shock protein system (HSP) is high frequency of losses and non-disjunction of sex chromosomes induced by heat shock (HS) (37 degrees C, 1 h). This effect was shown in only 6-14-th stages of oocytes. Anoxia was not effective in induction of these mutations. Successive action of anoxia and HS decreased loss frequency and non-disjunction in comparison with the only action of HS. These findings agree with the data in literature indicating that HSP synthesis was increased in the l(1)ts403 mutant when first anoxia and then HS were administered, in contrast to the action of HS only. The role of HSP in the recovery of HS-induced disruptions (chromosomal proteins and meiotic division apparatus) which can lead to chromosome non-disjunction and losses is discussed.