Sodium-potassium-dependent-ATPase activity in Emory mouse lens

Abstract

Previous morphological and biochemical studies indicate that a late appearing hereditary Emory mouse cataract may be a good model for certain human senile cataracts. The development of lenticular opacity in the Emory mouse is a slow process which provides an opportunity to conduct analysis of the progression of alterations that lead to cataract development. Biochemical investigations have not yet demonstrated any specific correlation between alterations in the lens and the extent of opacity. We have conducted studies to determine the role of Na+K+-ATPase in the development of cataract in the Emory mouse. In this report we present results obtained on the site and level of activity of Na+K+-ATPase in six- and twelve-month-old Emory mouse lenses in which visible cataractous changes are beginning to appear. CFW mice (the parent strain) were used for controls in this study. Ultrastructural cytochemistry for the localization of Na+-K+-ATPase exhibited the enzyme reaction product for this enzyme to be present mainly between the lateral epithelial cell membranes and between the apical epithelial cell membranes and superficial cortical fiber membranes. In cortical fibers the reaction product was localized between fiber membranes. Although there was very little or no significant differences in the extent of reaction product in epithelial cells, the reaction product in the cortical fibers of six-month-old Emory mouse was less extensively distributed as compared to lenses from control CFW mice of the same age.(ABSTRACT TRUNCATED AT 250 WORDS)

Sodium Pump Inhibition and Regional Expression of Sodium Pump α-Isoforms in Lens

“…[1][2][3][4][5][6][7][8] The mechanisms for this reduction in Na ϩ ,K ϩ -ATPase activity are not completely understood but could result from an endogenous inhibitor or reductions in functional sodium pump units. We have recently isolated a labile, endogenous Na ϩ ,K ϩ -ATPase inhibitor from the peritoneal dialysate of hypertensive renal failure patients.…”

“…2 Rodriguez-Sargent et al 2 recently reported that development of cataracts in Dahl S rats in response to a high salt diet can be predicted by a reduction in ouabain-sensitive Na ϩ ,K ϩ -ATPase activity several weeks before cataract formation. Likewise, a reduction in lens Na ϩ ,K ϩ -ATPase (sodium pump) activity occurs in several other animal models of cataract [2][3][4][5] and in human cataract formation. 3,6 -8 A similar reduction in sodium pump activity is also a common feature of hypertension and is thought to be mediated in part by a circulating sodium pump inhibitor 9 called either digitalis-like factor (DLF) or ouabain-like factor.…”

Regional changes of AQP0-dependent square array junction and gap junction associated with cortical cataract formation in the Emory mutant mouse

“…The Emory mutants develop late-onset light opacity around 7 months old and progressively turn into dense cataracts later at older age [Kuck et al, 1981; Kuck, 1990]. A number of biochemical and morphological studies have reported that many different changes are associated with the cataract formation [Kuck et al, 1981; Bhuyan et al, 1982; Swanson et al, 1985; Rathbun et al, 1986; Unakar et al, 1986; Lo and Kuck, 1987; DeNagel et al, 1988; Takemoto et al, 1988; Kuck and Kuck, 1989; Shi and Bekhor, 1992; Taylor et al, 1995; Reddy et al, 1999; Congdon et al, 2000; Sheets et al, 2002]. …”