Methylmercury intoxication and histochemical demonstration of NADPH-diaphorase activity in the striate cortex of adult cats

Abstract

The effects of methylmercury (MeHg) on histochemical demonstration of the NADPH-diaphorase (NADPH-d) activity in the striate cortex were studied in 4 adult cats. Two animals were used as control. The contaminated animals received 50 ml milk containing 0.42 µg MeHg and 100 g fish containing 0.03 µg MeHg daily for 2 months. The level of MeHg in area 17 of intoxicated animals was 3.2 µg/g wet weight brain tissue. Two cats were perfused 24 h after the last dose (group 1) and the other animals were perfused 6 months later (group 2). After microtomy, sections were processed for NADPHd histochemistry procedures using the malic enzyme method. Dendritic branch counts were performed from camera lucida drawings for control and intoxicated animals (N = 80). Average, standard deviation and Student t-test were calculated for each data group. The concentrations of mercury (Hg) in milk, fish and brain tissue were measured by acid digestion of samples, followed by reduction of total Hg in the digested sample to metallic Hg using stannous chloride followed by atomic fluorescence analysis. Only group 2 revealed a reduction of the neuropil enzyme activity and morphometric analysis showed a reduction in dendritic field area and in the number of distal dendrite branches of the NADPHd neurons in the white matter (P<0.05). These results suggest that NADPHd neurons in the white matter are more vulnerable to the long-term effects of MeHg than NADPHd neurons in the gray matter. Correspondence

<i>S</i>-Mercuration of cellular proteins by methylmercury and its toxicological implications

“…Because MTs have very high affinities for MeHg by virtue of the large numbers of thiol groups (-SH) content (Oliveira et al, 1998), the formation of MeHg-MT complexes may keep MeHg in a relatively nontoxic form, thereby protecting cells from the cytotoxic effects of MeHg (Aschner et al, 1997). Decreased concentrations of GSH and/or MT could cause cells to be more susceptible to the effects of MeHg (Hirooka et al, 2010), and the disturbances in cellular signal transduction pathways could cause adverse events including cell death.…”

Neuropil reactivity, distribution and morphology of NADPH diaphorase type I neurons in the barrel cortex of the adult mouse

“…NADPH-d, in the neocortex, is usually associated with GABAergic neurons (Valtschanoff et al, 1993) and has drawn interest since the demonstration that neurons containing this enzyme are resistant to injury mediated by many factors lethal to other cell groups (Thomas and Pearse, 1964;Ferrante et al, 1985), such as the excessive concentration of excitatory amino acids (Koh et al, 1986), malnutrition and intoxication by heavy metals (Oliveira et al, 1998). NADPH-d has also been characterized as a nitric oxide synthase (NOS) and has been used to identify neurons that express the neurotransmitter nitric oxide (NO) (Dawson et al, 1991;Hope et al, 1991), a gas which readily diffuses through both lipid and aqueous media and has a half-life of a few seconds (Vincent, 1994).…”

Neurotoxic Effects in Workers of the Clinical Thermometer Manufatcure Plant

“…Mercury exposure is associated with a wide range of central and peripheral nervous system dysfunctions [13], fine tremors in the fingers, eyelids and lips, which are early signs of mercury toxicity [14]. It has recently been suggested that Hg can impair the function of astrocytes with subsequent neuronal lesion [15] and lead to chronic neurotoxic effects [16]. Occupational exposure to mercury vapors may lead to neurological alterations [17], and chronic exposure may result in slowing of conduction velocity in long nerves [18].…”