Sodium nitrite alone protects the brain microsomal Ca(2+)-ATPase against potassium cyanide-induced neurotoxicity in rats.

The effect of a short-term oral administration of potassium cyanide (KCN) (200 ppm in diet) with or without sodium nitrite (NaNO2) pretreatment on rat brain microsomal Ca2 +/- ATPase was investigated. The specific activity value of the enzyme significantly decreased (p < 0.05) by 50% compared with control and by 63% for KCN-treated rats compared with KCN-treated rats pretreated with NaNO2. There was no significant difference at the h = 0.05 level between the values obtained for the control and KCN-treated rats pretreated with NaNO2. These results show both that feeding lowers brain microsomal Ca(2+)-ATPase activity and that NaNO2 has a protective role (antidote function) in that respect.

Reversal of sodium arsenite inhibition of rat liver microsomal Ca2+ pumping ATPase by vitamin C.

Sodium arsenite (NaAsO2), at 10% of its median lethal dose, was administered to rats with and without vitamin C pretreatment. Liver microsomal fraction was isolated and the activity of Ca2+-ATPase was assayed. Sodium arsenite was found to inhibit the activity of the liver microsomal Ca2+-ATPase to 50% to that of control rats. The specific activity of the enzyme in rats administered sodium arsenite with vitamin C pretreatment was not significantly different from that of control rats.

Iron-induced oxidative stress in erythrocyte membranes of non-insulin-dependent diabetic Nigerians.

The presence of higher level of endogenous free radical reaction products in the erythrocyte ghost membrane (EGM) of Non-insulin-dependent diabetes mellitus (NIDDM) subjects compared with that of normal healthy controls has been demonstrated. The EGMs of NIDDM subjects were also shown to be more susceptible to exogenously generated oxidative stress than those of normal healthy individuals. The decreased level of reactive thiol groups in the EGM of NIDDM individuals supported this observation. We propose that the presence of significant levels of non-heme iron in the EGM of NIDDM subjects is an indication of the potential for iron-catalysed production of hydroxy and other toxic radicals which could cause continuous oxidative stress and tissue damage. Oxygen free radicals could therefore be responsible for most of the erythrocyte abnormalities associated with non-insulin-dependent diabetes and could indeed be intimately involved in the mechanism of tissue damage in diabetic complications.

Active and passive smoking and risk of ovarian cancer.

It is unclear whether smoking is a risk factor for epithelial ovarian cancer, although some studies have suggested that it may be associated with an increased risk of mucinous tumors. This study investigated the effect of smoking and environmental tobacco smoke (ETS) on ovarian cancer risk among 434 women with primary epithelial ovarian, peritoneal, or fallopian cancers and 868 age- and region-matched hospital controls with nonneoplastic conditions. All participants completed a comprehensive epidemiologic questionnaire. Results indicate that decreased risk of ovarian cancer was associated with being a nonsmoker exposed to ETS (adjusted odds ratio [aOR] 0.68, 95% confidence interval [CI] 0.46-0.99), a former smoker (aOR 0.76, 95% CI 0.53-1.10), or a current smoker (aOR 0.53, 95% CI 0.32-0.88). A similar protective effect was noted for smokers with moderate or high exposure based on smoking intensity, duration, and cumulative exposure, as well as for never smokers exposed to ETS. Results did not differ substantially by histologic subtype. Although prevailing theories of ovarian cancer etiology implicate incessant ovulation, characteristics of the study population suggest that anovulation was not the protective mechanism in this study. Immunosuppression by nicotine or upregulation of enzymes that metabolize carcinogens may be responsible for the effects observed.

Hop: more than an Hsp70/Hsp90 adaptor protein.

Molecular chaperones facilitate the correct folding of other proteins under physiological and stress conditions. Recently it has become evident that various co-chaperone proteins regulate the cellular functions of these chaperones, particularly Hsp70 and Hsp90. Hop is one of the most extensively studied co-chaperones that is able to directly associate with both Hsp70 and Hsp90. The current dogma proposes that Hop functions primarily as an adaptor that directs Hsp90 to Hsp70-client protein complexes in the cytoplasm. However, recent evidence suggests that Hop can also modulate the chaperone activities of these Hsps, and that it is not dedicated to Hsp70 and Hsp90. While the co-chaperone function of Hop within the cytoplasm has been extensively studied, its association with nuclear complexes and prion proteins remains to be elucidated. This article will review the structural features of Hop, and the evidence that its biological function is considerably broader than previously envisaged.