Involvement of endometrial membrane sulphydryl groups in blastocyst implantation: sulphydryl groups as a potential target for contraceptive research.

The role of membrane sulphydryl groups in blastocyst implantation was studied by masking the membrane sulphydryl groups in the endometrium of Swiss albino mice, Mus musculus, using 10(-5) M cobalt chloride and 0.05 mM as well as 0.005 mM n-ethylmaleimide. Here we show that the blocking of sulphydryl groups with cobalt resulted in a decrease in superoxide radical surge and an increase in superoxide dismutase levels at the time of implantation. We hypothesize that it may be due to either a decrease in membrane fluidity or the unavailability of sulphydryl groups of endometrial membrane, thus preventing blastocyst implantation. These sulphydryl groups can be targeted for future contraceptive research.

Restoration of methylmercury inhibited adenosine triphosphatases during vitamin and monothiol therapy.

The aim of our investigation was to examine the efficacy of monothiols and vitamins in the restoration of ion-dependent ATPases in mice intoxicated with methylmercury chloride (MMC). A daily dose of glutathione (GSH), N-acetyl-DL-homocysteine thiolactone (NAHT), vitamin B complex, or vitamin E, either alone or in combination, resulted in significant recovery of N+, K+, Mg++ ATPases. A significant recovery was noted in some therapeutic groups. As the therapeutic agents used in this study are natural physiological components present in all the animals, they are unlikely to be injurious if applied in appropriate doses. Hence, they can be safely recommended for methylmercury detoxication.

Vitamins and monothiols efficacy in the restoration of adenosine nucleotide degradation enzymes altered during methylmercury intoxication.

Male albino mice were intoxicated with a daily dose of 1 mg/kg of methylmercury chloride (MMC) for 7 days, and were treated thereafter with glutathione, N-acetyl-DL-homocysteine thiolactone, vitamin B complex, and vitamin E, either alone or in combinations, for the next 7 days. The animals were sacrificed on the eighth day, with the exception of one group that was kept without toxic exposure for an additional 7 days and sacrificed on the fifteenth day. Brain, spinal cord, kidney, and liver of the animals were examined for changes in adenosine deaminase and 5' nucleotidase. We found a severe inhibition of these enzymes during MMC intoxication and significant recovery during monothiols and vitamins administration, indicating the effectiveness of these agents in methylmercury detoxication.

Fluctuation of trace elements during methylmercury toxication and chelation therapy.

The aim of the present investigation was to check the fluctuation in essential elements, such as Na, K, Mg, Mn, Cu, Zn, Cr and Ni in the brain, spinal cord, liver and kidney of mice during methylmercury chloride (MMC) toxication and therapy with monothiols (N-acetyl-DL-homocysteine thiolactone and glutathione) and vitamins (vitamin B complex and E). Mercury deposition and its elimination during chelation therapy were also screened for comparative purposes. The animals were dosed for 7 days with MMC 1 mg/kg/d and some were then kept without treatment for a further. 7 days. Other MMC-treated animals were immediately given one of the above antidotes for 7 days. All the animals were sacrificed on the 15th day. There was a decrease in all elements during MMC toxication with few exceptions, for example, copper was increased in the liver as was sodium in the kidney. Treatment with the thiols and vitamins restored the levels of these elements in certain tissues towards normal, but their concentrations remained abnormal in most instances. The fluctuations in the concentration of these elements were attributed to their association with various macromolecules.

Acetylcholinesterase fluctuations in central nervous system of rat during methylmercury intoxication and chelation therapy.

A daily dose of 1 mg/kg and 10 mg/kg of methylmercury chloride (MMC) was injected to separate sets of rats for 2 days, 7 days, and 15 days. Low and high doses of four MMC antagonists, namely N-acetyl-DL-homocysteine thiolactone (NAHT), glutathione (GSH), D-penicillamine (DPA), and sodium selenite (SEL) were injected intramuscularly (i.m.) to MMC-treated animals after an interval of half an hour. The animals were sacrificed on the 3rd, 8th, and 16th day, respectively. An additional group of rats was treated with MMC for 7 days; thereafter, it was kept free of toxic exposure for 7 days and sacrificed on the 15th day. The brain was dissected and separated into olfactory bulbs, cerebral hemispheres, cerebellum, and medulla oblongata. Each part of the central nervous system (CNS) was studied separately. We found a dose- and duration-related acetylcholinesterase (AChE) inhibition in all CNS areas. The use of antagonists showed different effects in different CNS areas, but no appreciable recovery of AChE activity could be obtained with the doses used.

Ameliorative capacities of vitamins and monothiols administered alone or in combinations in methylmercury mobilisation in nervous and non-nervous tissues of mice.

The extent of mercury mobilisation was recorded from various tissues (brain, spinal cord, liver and kidney) of male mice administered with a daily dose of methylmercury chloride (1 mg/kg) for seven days. For this purpose 10 groups of animals were intoxicated. Out of these, one group was sacrificed on 8th day and one group was kept without toxicant for another seven days before sacrificing on 15th day. To the rest of the groups were given a daily dose of N-acetyl-DL-homocysteine thiolactone (NAHT), glutathione (GSH), vitamin B Complex and E, applied either alone or in combinations. All these animals were sacrificed on the 15th day. The mercury clearance rate during thiols, vitamins and their co-administration was examined. Study shows that both the vitamins were able to increase mercury elimination from the nervous and non-nervous tissues. Their combination with NAHT was not suitable as mercury level was increased in all the tissues except kidney as compared to NAHT alone treated group. However, vitamin B Complex combination with glutathione was much advantageous. It is concluded from the overall study that application of vitamin B Complex and E either alone or in combination with GSH is quite suitable for methylmercury post-therapy.

Inefficiency of metal chelators to promote recovery of methylmercury inhibited CNS succinic dehydrogenase.

This paper deals with the level of succinic dehydrogenase (SDH) in various locations of the central nervous system (CNS) of rat, treated with methylmercury chloride (MMC) and later with antagonists. None of the CNS areas reveals any effect after 2 days of MMC application, but further treatment causes a linear inhibition of the enzyme with increasing duration of MMC exposure. Maximal inhibition in all regions is exhibited after 15 days of treatment. In absolute terms, the maximal inhibition is observed in the olfactory bulbs and the minimal effect is seen in the spinal cord after 15 days with low and high doses of MMC respectively.