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Abstract: Effects of treatment with a single intra-peritoneal (i.p.) injection (0.84mgCd/kg body weight) of cadmium (Cd) on lipid/phospholipids profiles of rat brain microsomes and mitochondria were examined. At the end of one-week following treatment with Cd the microsomal total phospholipids (TPL) content was unchanged but the cholesterol (CHL) content increased. In one-month Cd-treated group both TPL and CHL contents increased. In one-week Cd-treated group the content of phosphatidylinositol (PI) decreased whereas that of lysophospholipid and phosphatidic acid (PA) increased. In one-month Cd-treated group the sphinghomyelin (SPM) and phosphatidycholine (PC) components increased whereas phosphatidyethanolamine (PE) and PA decreased. In mitochondria, CHL content increased in both Cd-treated groups. The content of TPL decreased only in one-month Cd-treated group. In one-week Cd-treated group the lysophospholipids increased whereas PI and phosphatidylserine (PS) decreased. In one-month group the lysophospholipids, PI and diphosphatidylglycerol (DPG) components decreased whereas PS and PE component increased. The results suggest that exposure to a single dose of Cd has differential and long-lasting effects on lipid/phospholipids profiles of rat brain microsomes and mitochondria. [Copyright &y& Elsevier]

Abstract: Objectives: : Effects of treatment with dehydroepiandrosterone (DHEA) on oxidative energy metabolism in rat liver and brain mitochondria were examined. Design and methods: : Young adult rats were administered DHEA (0.1, 0.2, 1.0 or 2.0 mg/kg body weight) by subcutaneous route for 7 consecutive days. Results: : DHEA treatment resulted in general, in stimulation of state 3 respiration rates without having any uncoupling effect on ADP/O ratios. The stimulation of state 3 respiration rate for a given substrate was dose dependent in a tissue-specific manner. Parallel increases in the contents of cytochromes aa3 and b were also noted. DHEA treatment stimulated the glutamate dehydrogenase (GDH) and succinate DCIP reductase (SDR) activities. Under the treatment conditions, mitochondrial ATPase activity was also stimulated. Conclusions: : Treatment with DHEA significantly stimulated oxidative energy metabolism in liver and brain mitochondria. [Copyright &y& Elsevier]

Abstract: Effect of neonatal hypothyroidism on kinetic properties of Ca2+-ATPase from rat brain synaptic plasma membranes and microsomes were examined. Neonatal hypothyroidism resulted in significant decrease in the enzyme activity in both the membrane systems. The synaptic membranes in control group displayed presence of one kinetic component whereas a low affinity component became evident in the hypothyroid group. In the microsomes, both control as well as hypothyroid groups showed presence of two kinetic components with the latter group showing two-fold increase in the K m. The Ca2+ binding characteristics were generally unaltered in the enzyme from both the membrane systems. Our results suggest that impairment in the Ca2+-ATPase activity together with altered kinetic properties could be one of the underlying biochemical mechanisms leading to CNS dysfunction as a consequence of thyroid hormone deprivation during critical stages of brain development. [Copyright &y& Elsevier]

Abstract: Studies on Cd hepatotoxicity have focused mainly on induction of cytochrome P450 system and related enzymes. In the present study young adult male rats given a single intra-peritoneal injection of Cd (0.84mg Cd/kg body weight) and effects on kinetic parameters rat liver microsomal Na+, K+-ATPase and G6Pase were evaluated at the end of 1 month and 1 week. The substrate and temperature kinetics parameters were examined and attempts were made to seek correlation with changes in lipid/phospholipid profiles. The Na+, K+ ATPase activity decreased only in 1 week Cd-treated group but recovered at the end of 1 month. The activity resolved in two distinct kinetic components in control as well as the experimental groups. In 1 week Cd-treated group the K m value of both the components was unchanged, whereas V max value decreased. In 1-month Cd-treated group V max value only of component I increased. The catalytic efficiency of both the components was not affected in the experimental groups. In 1-week Cd-treated group the energy of activations at high-temperature range (E H) and low-temperature range (E L) decreased, whereas for 1-month Cd-treated group the energies of activations did not change. The G6Pase activity measured at 37°C was high only in 1-month Cd-treated group. The activity resolved in two kinetically distinguishable components in control as well as in the experimental groups. K m value of component I decreased in both the Cd-treated groups. In 1-month Cd-treated group the V max value of component II increased. The catalytic efficiency of G6Pase was unchanged despite changes in K m and V max. In 1-week Cd-treated group the E H and E L decreased, whereas only E L showed decrease in 1-month Cd-treated group. Cholesterol (CHL) content increased in both the Cd-treated groups. Content of lysophospholipid (Lyso), spinghomyelin (SPM) and phosphatidic acid (PA) increased, whereas phosphatidylcholine (PC) and phosphatidylserine (PS) decreased in 1-week Cd-treated group. In 1-month Cd group the Lyso, SPM, and PC increased while PC, phosphatidylethanolamine (PE) and PA decreased. In conclusion, Cd has short-term effects on microsomal Na+, K+-ATPase which are reversed by the end of 1 month and that G6Pase does not seem to be a target of Cd insult. [Copyright &y& Elsevier]

Effect of long-term (90-100 days) exposure of rats to soluble salt of aluminum (AlCl3) on myelin lipid profile was examined. The long-term exposure to AlCl3 resulted in a 60 % decrease in the total phospholipid (TPL) content while the cholesterol (CHL) content increased by 55 %. Consequently the TPL / CHL molar ratio decreased significantly by 62 %. The phospholipid composition of the myelin membrane changed drastically; the proportion of practically all the phospholipid classes decreased by 32 to 60 % except for phosphatidylcholine (PC) and phosphatidylethanolamine (PE). Of the latter two, proportion of PC was unchanged while PE increased in proportion by 47 %. Quantitatively, all phospholipid classes decreased by from 42 to 76% with no change in the PE content. However the membrane fluidity was not altered in Al-treated rats. Many of the changes we observe here show striking similarities with the reported phospholipid profiles of Alzheimer brains. [ABSTRACT FROM AUTHOR]

Early and late effects of alloxan diabetes and subsequent treatment with insulin on the temperature kinetics properties of succinate oxidase (SO) activity in rat kidney mitochondria were examined. In diabetic animals SO activity increased significantly and the increase was more pronounced at the late stage. Insulin treatment partially restored SO activity. However, the effect was temperature-dependent. In diabetic animals the energy of activation in the low temperature range (E(L)) increased significantly while that in the high temperature range (E(H)) decreased. The latter seems to be responsible for improving catalytic efficiency in the diabetic state. Insulin treatment normalized E(H) only in the 1-month diabetic group. The phase transition temperature (Tt), decreased in diabetic animals. Insulin treatment caused an increase beyond the control value in Tt in 1-month diabetic animals. The results suggest that insulin status-dependent modulation of SO activity is a complex process. [ABSTRACT FROM AUTHOR]