Effects of in vitro exposure to mercury on male gonads and sperm structure of the tropical fish tuvira Gymnotus carapo (L.).

This study investigated the progressive effects of HgCl2 in the testis and sperm of the tropical fish tuvira Gymnotus carapo L. exposed to increasing Hg concentrations (5-30 µm) and increasing exposure times (24-96 h). Histopathology and metal concentrations in the testis were observed. Hg concentrations in the testis reached 5.1 and 5.2 µg g(-1) in fish exposed to 20 and 30 µm of Hg, respectively. Hg effects on testicular tissue were observed even at low Hg concentrations, with no alterations in gonadosomatic index. However, the quantitative analysis of the induced alterations (lesion index) demonstrated that the Hg effects in testis became more severe after exposure to higher concentrations (20 and 30 µm) and during longer exposure (72 and 96 h), probably leading to partial or total loss of the organ function. Hg exposure (20 µm) also affected sperm count and altered sperm morphology. This study showed that HgCl2 caused progressive damage to testicular tissue, reduced sperm count and altered sperm morphology. These results are important in establishing a direct correlation between Hg accumulation and severity of lesions.

Organotropism of methylmercury in fish of the southeastern of Brazil.

This is one of the first studies to evaluate the effect of biometric variables (total length and weight), diet, and abiotic matrices (sediment and water column) on the bioaccumulation of methylmercury in tissues (muscle, liver, and gills) of four fish (two carnivore-invertivores, Pimelodus fur and Pachyurus adspersus; one carnivore-piscivore, Oligosarcus hepsetus; and one omnivore, Pimelodella lateristriga) in the lower section of a river in southeastern Brazil. Samples of fish (n = 120), water (n = 5) and sediment (n = 5) were collected at five sites characterized by pollution with mercury due to the use of organomercury fungicides and stream bed gold mining, commonly carried out in that section of the river in the 1980s. The results show that biometric variables are strongly correlated with methylmercury levels in muscle (r = 0.61, p < 0.0005) of P. fur. As a rule, concentrations of total mercury and methylmercury did not vary considerably between the organs of the species of different food habits, because of the environmental conditions in the study area. Despite the low concentrations of mercury in sediments (<0.05 mg kg-1 wet. wt), this compartment is a representative source of this pollutant for the organisms investigated, due to the close contact these animals keep with it in view of the low water columns in that section of the river.

Mercury-induced dysfunctions in multiple organelles leading to cell death.

Mercury (Hg) is a highly toxic metal that can exert multiple adverse effects, ultimately leading to cell death. Before causing death, the Hg enters the cells and affects diverse intracellular targets. The present study aimed to investigate the structure and function of several organelles or cellular structures, including mitochondria, acidic compartments and vesicles, endoplasmic reticulum elements and microfilaments, following Hg exposure of a human hepatic cell line (HuH-7 cells) to examine the sequence and coordination of the events associated with Hg-induced cell death. Hg exposure led to a progressive decrease in cell viability and induced alterations in cell morphology including cytoplasmic shrinkage and nuclear fragmentation. Hg treatment (10 µM for 12 h) affected multiple intracellular targets simultaneously. These included loss of mitochondrial functionality, pronounced cytoplasmic acidification and dysfunctions in the cytoskeleton and endoplasmic reticulum. This overall Hg-induced toxicity in the human hepatocyte cell line (HuH-7 cells) led to cell death through both apoptosis and autophagy.

Evolution of cadmium effects in the testis and sperm of the tropical fish Gymnotus carapo.

The present study investigated the testis and sperm morphology of the tropical fish Gymnotus carapo after exposure to increasing CdCl2 concentrations (5-40 µM) for 24 and 96 h. The treatments induced Cd accumulation in the testis and a decrease in the gonadosomatic index from a 10 µM. Cd induced alterations in testis since 24h; however the extension and severity of damages increased after 96 h in all tested concentrations. Marked variations in the cysts size, proliferation of the interstitial tissue, infiltration of inflammatory cells, necrosis, reduction of germ cells and sperm aggregation was observed in 96 h treated fishes. In this time, there was a complete absence of germ cells in the testis of fish treated with 40 µM. The ultrastructural analysis allowed for the visualization of the initial damages over germ cells, such as the presence of vacuoles in the cytoplasm of spermatogonia, spermatocytes, and spermatids. Exposed fish (20 µM for 24 and 96 h) had alterations in sperm number and morphology. These results are important for establishing a direct correlation between the Cd accumulation and incidence of damages and can help characterize the mechanism of Cd-induced pathogenesis in the male reproductive system.

Autophagy, apoptosis and organelle features during cell exposure to cadmium

Cadmium (Cd) induces several effects in different tissues, but our knowledge of the toxic effects on organelles is insufficient. To observe the progression of Cd effects on organelle structure and function, HuH-7 cells (human hepatic carcinoma cell line) were exposed to CdCl2 in increasing concentrations (1 microM - 20 microM) and exposure times (2 h - 24 h). During Cd treatment, the cells exhibited a progressive decrease in viability that was both time- and dose-dependent. Cd treated cells displayed progressive morphological changes that included cytoplasm retraction and nuclear condensation preceding a total loss of cell adhesion. Treatment with 10 microM for 12 h led to irreversible damages. Before these drastic and irreparable damages, treated cells (5 microM for 12 h) presented a progressive loss of mitochond rial function and cytoplasm acidification as well as dysfunction and disorganization of microfilaments and endoplasmic reticulum. These damages led to the induction of apoptotic events and an increase in autophagic bodies in the cytoplasm. These results revealed that Cd affects multiple intra-cellular targets that induce alterations in the mitochondria, cytoskeleton, endoplasmic reticulum and acidic compartments, ultimately culminating in cell death via apoptotic and autophagic pathways.