Organ-specific accumulation of selenium and mercury in Indo-Pacific bottlenose dolphins (Tursiops aduncus).

Delphinids are top ocean predators and accumulate high concentrations of mercury (Hg) through the food chain, particularly in organs such as liver and kidney, although the proportion of methylmercury (MeHg) is relatively low due to the demethylation process. Total mercury (T-Hg) levels in marine mammals have been shown to correlate with selenium (Se) concentrations, and ingested MeHg that is demethylated may be present in tissues as mercury selenide (HgSe). In this study, we determined T-Hg, MeHg and Se concentrations of three Indo-Pacific bottlenose dolphins (Tursiops aduncus), and we used the individual with the highest Hg concentration for electron probe microanalysis to assess the co-localization of Hg and Se in the tissues.

Breast milk contribution to tissue mercury levels in rat pups examined by cross-fostering at birth.

The developing perinatal brain is vulnerable to methylmercury (MeHg) exposure. The contribution of breast milk to tissue MeHg levels in offspring is a significant public health concern because breast milk contains a certain amount of MeHg. Here, the contribution of MeHg transferred via breast milk to the Hg levels in the tissues of pups (Wistar rats) was investigated.

Mercury and Selenium Localization in the Cerebrum, Cerebellum, Liver, and Kidney of a Minamata Disease Case.

Minamata disease is a methylmercury poisoning caused by consumption of marine food contaminated by man-made methylmercury environmental pollution, and its most prominent feature is marked pathological changes in the central nervous system. Morphological alterations are less pronounced in the liver and the kidney, although their mercury levels are higher than those of the brain. In marine mammals, methylmercury is known to be easily converted to inorganic mercury and it combines with selenium forming mercury selenide, which may counteract the toxicity of mercury.

Application of the Quartz Crystal Microbalance Method for Measuring Mercury in the Air of Working Environments Involved to Artisanal and Small-scale Gold Mining (ASGM).

Artisanal small gold mining (ASGM) is responsible for approximately 40% of the total Hg emissions into the atmosphere worldwide. In developing countries, many people are engaged in ASGM activities. We developed a small, simple Hg measuring device, which detects Hg in the air based on the change of the oscillation frequency of an Au electrode on a quartz crystal microbalance (QCM).

Neuropathology associated with exposure to different concentrations and species of mercury: A review of autopsy cases and the literature.

Background: Human exposure to mercury (Hg) is widespread and both organic and inorganic Hg are routinely found in the human brain. Millions of people are exposed to methyl Hg (MeHg) due to the consumption of fish and to inorganic Hg from dental amalgams, small scale gold mining operations, use of Hg containing products, or their occupations. Neuropathology information associated with exposures to different species of Hg is primarily based on case reports of single individuals or collections of case studies involving a single species of Hg at toxic exposure levels such as occurred in Japan and Iraq.

Mercury speciation in preserved historical sludge: Potential risk from sludge contained within reclaimed land of Minamata Bay, Japan.

In the latter half of the 1950s, a large amount of methylmercury (MeHg) was discharged directly into Minamata Bay, Japan by a chemical factory, resulting in the contamination of the fish and shellfish. Ultimately, an outbreak of MeHg intoxication, called Minamata disease, occurred. From 1977 to 1988, the Kumamoto Prefectural Government dredged and transferred sediments exceeding 25 μg/g of total mercury (THg, dry basis) into a strictly segregated area of the bay near the wastewater outlet, then this area was landfilled.

Mercury speciation and selenium in toothed-whale muscles.

Mercury accumulates at high levels in marine mammal tissues. However, its speciation is poorly understood. The main goal of this investigation was to establish the relationships among mercury species and selenium (Se) concentrations in toothed-whale muscles at different mercury levels.

Dietary mercury exposure resulted in behavioral differences in mice contaminated with fish-associated methylmercury compared to methylmercury chloride added to diet.

Methylmercury (MeHg) is a potent neurotoxin, and humans are mainly exposed to this pollutant through fish consumption. However, in classical toxicological studies, pure methylmercury chloride (MeHgCl) is injected, given to drink or incorporated within feed assuming that its effects are identical to those of MeHg naturally associated to fish. In the present study, we wanted to address the question whether a diet containing MeHg associated to fish could result in observable adverse effects in mice as compared to a diet containing the same concentration of MeHg added pure to the diet and whether beneficial nutriments from fish were able to counterbalance the deleterious effects of fish-associated mercury, if any.

Methylmercury inhibits electron transport chain activity and induces cytochrome c release in cerebellum mitochondria.

The involvement of oxidative stress has been suggested as a mechanism for toxicity caused by methylmercury (MeHg). One of the major critical sites for oxidative stress is the mitochondria. In this research, to clarify the target site in mitochondria affected by MeHg, the individual activities of the mitochondrial electron transport chain (ETC) (I∼IV) were examined in the liver, cerebrum and cerebellum of MeHg-intoxicated rats.

Effect of methylmercury administration on choroid plexus function in rats.

Methylmercury (MeHg) is a well-known environmental neurotoxin. The choroid plexus (CP), the main component of the blood-cerebrospinal fluid (CSF) barrier (BCSFB), protects the brain from xenobiotics, similar to the blood-brain barrier. Because CP is considered a critical target site of MeHg-induced neurotoxic damage, functional alterations in CP may be caused in relation to the extent of MeHg-induced brain injury.

Neurotoxic action of inorganic mercury injected in the intraventricular space of mouse cerebrum.

To examine the neurotoxic action of inorganic mercury, HgCl(2) was injected in the intraventricular space of a mouse brain as a mimic for an Hg(0) vapor-exposed model, and the Hg distribution in the brain and behavioral changes were compared with those of Hg(0)-exposed mice. Although no difference was found in the Hg accumulation and its localization in the brains of two model mice at 3 weeks after Hg treatment, the turnover rate of the brain Hg in the Hg(0)-exposed mice was higher than in the Hg(II)-injected mouse. Despite a similar Hg level in the cerebrum at 3 weeks, behavioral alterations, hyper-activity in an open field test and shortening of latency in a passive avoidance test, were significant only in Hg(II)-injected mice.

The pathology of methylmercury poisoning (Minamata disease): The 50th Anniversary of Japanese Society of Neuropathology.

Methylmercury (Me-Hg) poisoning (Minamata disease: MD) is one of the most severe types of disease caused by humans to humans in Japan. The disease is a special class of food-borne methylmercury intoxication in humans as typified by the outbreak that began in 1953 in Minamata and its vicinity in Kumamoto Prefecture, Japan. There are 450 autopsy cases in Kumamoto and 30 autopsy cases in Niigata Prefecture related to MD in Japan.