Effects of lindane on the glucose metabolism in rat brain cortex cells

Pulido, J.A.; Hoyo, N. del; Pérez-Albarsanz, M.A.

doi:10.1016/0024-3205(90)90168-q

Cited by 8 publications

(1 citation statement)

References 30 publications

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“…In addition, multiple effects not mediated by GABA A receptors have been described after in vitro exposure to lindane. Those include: alterations of the plasma membrane (Kang and Yun, 1994) and of glucose metabolism (Pulido et al, 1990), increases in the formation of inositol phosphate (Cristòfol et al, 1993), changes of the intracellular calcium concentration (Bondy and Halsall, 1988;Joy and Burns, 1988;Ferguson and Audesirk, 1995;Rosa et al, 1997), alterations of neurite development (Ferguson and Audesirk, 1995), and modulation of c-fos expression (Barrón et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Cytotoxic action of lindane in neocortical GABAergic neurons is primarily mediated by interaction with flunitrazepam-sensitive GABAA receptors

Vale

Damgaard²,

Suñol

et al. 1998

J. Neurosci. Res.

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The cytotoxic action of the gamma-isomer of hexachlorocyclohexane (y-HCH; lindane) was studied in cultured mouse neocortical neurons by measurements of the reduction in mitochondrial function using the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) test. The cells were exposed to 30-300 microM lindane in the culture medium for different periods of time and lindane cytotoxicity was found to be time- and concentration-dependent. Lindane cytotoxicity could be ameliorated by addition of gamma aminobutyric acid (GABA) in a concentration-dependent manner but this effect of GABA was not blocked by bicuculline or picrotoxinin (PTX). Lindane induced cytotoxicity was also reduced by the GABA(A) receptor agonists muscimol and THIP (4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol). This effect was enhanced by the simultaneous presence of flunitrazepam but only at the highest lindane concentrations studied (200 and 300 microM). Flunitrazepam by itself had no effect on lindane-induced cytotoxicity. The protective effect of GABA plus flunitrazepam was blocked by the benzodiazepine receptor antagonist flumazenil and by the GABA(A) antagonist bicuculline, suggesting the involvement of central benzodiazepine receptors allosterically coupled to the GABA recognition site at the GABA(A) receptor. When 100 microM PTX was used to suppress the protective effect of GABA and flunitrazepam, a significant effect of PTX was observed only at 300 microM lindane. The GABA(B) receptor agonist, baclophen, only marginally reduced the cytotoxic effect induced by the highest lindane concentrations. It is concluded that the cytotoxic action of lindane in neocortical neurons in culture is mediated primarily through an interaction with allosterically coupled GABA-benzodiazepine recognition sites at the GABA(A) receptor.

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Section: Introductionmentioning

confidence: 99%

Cytotoxic action of lindane in neocortical GABAergic neurons is primarily mediated by interaction with flunitrazepam-sensitive GABAA receptors

Vale

Damgaard²,

Suñol

et al. 1998

J. Neurosci. Res.

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Lindane-induced modifications to membrane lipid structure: Effect on membrane fluidity after subchronic treament

Gutierrez-Ocaña¹,

Senar²,

Pérez-Albarsanz³

et al. 1992

Bioscience Reports

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Chronic lindane intoxication by injecting subcutaneously the toxicant, resulted in an altered lipid pattern in rat ventral prostate membranes. An increase of membrane fluidity was also observed using a fluorescence polarization technique. When in vitro experiments were carried out with both treated and untreated rats, an interesting lack of parallelism was found, which could indicate the development of a resistance to membrane disordering by lindane. The observed changes in cholesterol and phospholipid composition are also consistent with the hypothesis that lindane perturbs the lipid matrix of membranes, possibly inducing complex compensatory changes in the membrane lipid composition.

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Characterization of phosphoinositide hydrolysis products induced by hexachlorocyclohexane isomers in rat brain cortex

1993

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Water-soluble inositol metabolites were separated by anion-exchange chromatography in order to determine whether or not gamma-hexachlorocyclohexane (gamma-HCH, lindane) and related compounds affect phosphatidylinositol hydrolysis in rat brain cortex slices. Hydrolysis was increased by delta- and gamma-HCH, while alpha- and beta-HCH were inactive. Muscarinic receptor stimulation of rat cortical slices with carbachol increases inositol phosphates formation. The combined effect of carbachol and the hexachlorocyclohexane isomers together were approximately equal to the sum of the effect of each one separately. The results suggest that lindane stimulates phosphoinositide phospholipase C and/or inhibits the phosphatases implicated in dephosphorylation of inositol phosphates.

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Effects of lindane on the glucose metabolism in rat brain cortex cells

Cited by 8 publications

References 30 publications

Cytotoxic action of lindane in neocortical GABAergic neurons is primarily mediated by interaction with flunitrazepam-sensitive GABAA receptors

Cytotoxic action of lindane in neocortical GABAergic neurons is primarily mediated by interaction with flunitrazepam-sensitive GABAA receptors

Lindane-induced modifications to membrane lipid structure: Effect on membrane fluidity after subchronic treament

Characterization of phosphoinositide hydrolysis products induced by hexachlorocyclohexane isomers in rat brain cortex

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