Chalcobamba is a Cu-skarn deposit (338 Mt @ 0.55 % Cu) located in the centre of the Middle Eocene-Early Oligocene Las Bambas district, Andahuaylas-Yauri Belt, Southern Peru. At Chalcobamba, skarns formed when limestones of the Ferrobamba Formation were intruded by a Late Eocene quartz-diorite pluton. Skarn ores were then cut by a quartz monzodiorite porphyry stock, and swarms of monzogranitic and monzodiorite dikes.
Chalcobamba has spectacular outcrops of massive magnetite, massive epidote endoskarns, and coarse grained garnet. Magnetite and epidote display a wide range of textures linked with the evolution of alteration and mineralization in the deposit.
Distinctive magnetite textures formed during magmatic-hydrothermal activity in the intrusive rocks and in the prograde and retrograde skarn assemblages. The pluton, stocks and dikes typically have mafic minerals replaced by magnetite. Early banded magnetite and diopside skarn formed in limestone horizons that have some dolomitic content. Magnetite bands are typically thin and fine grained, but locally coarsen and increase in thickness. Magnetite associated with retrograde sulfide mineralization has replaced garnet and pyroxene in a continuous progression from magnetite patches to massive magnetite skarns. Hematite-epidote-calcite is a typical late-stage assemblage. In many cases, the hematite is partially to total pseudomorphed by magnetite, producing mushketovite. Some mushketovite crystals are up to 5 cm in diameter.
The typical epidote progression in intrusive rocks at Chalcobamba is from veinlets and disseminations in plutons, stocks and dikes, through endoskarn alteration patches, to tens of meter outcrops of massive epidote endoskarns. The monzogranitic swarm dike has a mappable gradient in disseminated epidote intensity. It is abundant near the skarn mineralization centre, and progressively weaker to the periphery of the system. The disseminated epidote consists of partial or total replacements of feldspars crystals. Epidote has also locally replaced prograde garnet, pyroxene and magnetite skarns. When epidote is associated with calcite and mushketovite, it typically displays coarse radial acicular textures.
Both magnetite and epidote have the capacity to record chemical anomalies via their stable isotopic or trace element compositions, potentially allowing inferences about the evolution and fertility of hydrothermal fluids to be made, provided that interpretations are made within the framework of the textural evolution of these key gangue minerals. Work is on-going to establish if any of the textural varieties of magnetite and/or epidote can be used to aid skarn exploration in the Andahuaylas-Yauri Belt, particularly as to whether mapping characteristic textures can provides insights into ore genesis and/or proximity to the center of mineralization.
Particulate hexavalent chromium (Cr(VI)) is a well-established human lung carcinogen. Lung tumors are characterized by structural and numerical chromosome instability. Centrosome amplification is a phenotype commonly found in solid tumors, including lung tumors, which strongly correlates with chromosome instability. Human lung cells exposed to Cr(VI) exhibit centrosome amplification but the underlying phenotypes and mechanisms remain unknown. In this study, we further characterize the phenotypes of Cr(VI)-induced centrosome abnormalities. We show that Cr(VI)-induced centrosome amplification correlates with numerical chromosome instability. We also show chronic exposure to particulate Cr(VI) induces centrosomes with supernumerary centrioles and acentriolar centrosomes in human lung cells. Moreover, chronic exposure to particulate Cr(VI) affects the timing of important centriolar events. Specifically, chronic exposure to particulate Cr(VI) causes premature centriole disengagement in S and G2 phase cells. It also induces premature centrosome separation in interphase. Altogether, our data suggest that chronic exposure to particulate Cr(VI) targets the protein linkers that hold centrioles together. These centriolar linkers are important for key events of the centrosome cycle and their premature disruption might underlie Cr(VI)-induced centrosome amplification.
Water-insoluble hexavalent chromium compounds are well-established human lung carcinogens. Lead chromate, a model insoluble Cr(VI) compound, induces DNA damage, chromosome aberrations, and dose-dependent cell death in human and Chinese hamster ovary (CHO) cells. The relationship between lead chromate–induced DNA damage and chromosome aberrations is unknown. Our study focus was on examining the role of XRCC1 in lead chromate–induced cytotoxicity and structural chromosomal aberrations in CHO cells. Three different cell lines were used: AA8 (parental), EM9 (XRCC1 mutant), and H9T3 (EM9 complemented with human XRCC1 gene). Cytotoxicity was significantly higher in EM9 cells when compared to AA8 and H9T3 cells, indicating that XRCC1 is important for protecting cells from lead chromate particles–induced cell death. The frequency of damaged metaphase cells was not affected by XRCC1 deficiency. However, the total amount of Cr(VI)-induced chromosome damage was exacerbated by XRCC1 deficiency, and the spectrum of damage changed dramatically. Chromatid and isochromatid lesions were the most prominent aberrations induced in all cell lines. XRCC1 was essential to reduce the formation of chromatid lesions, but not for isochromatid lesions. In addition, XRCC1 deficiency resulted in a dramatic increase in the number of chromatid exchanges, indicating that XRCC1 is involved in protection from lead chromate–induced chromosome instability.
Abstract The northern Gulf of Mexico has a long history of polycyclic aromatic hydrocarbon (PAH) contamination from anthropogenic activities, natural oil seepages, and the 2010 Deepwater Horizon explosion and oil spill. The continental shelf of the same area is a known breeding ground for sperm whales (Physeter macrocephalus). To evaluate PAH-DNA damage, a biomarker for potential cancer risk, we compared skin biopsies collected from Gulf of Mexico sperm whales in 2012 with skin biopsies collected from sperm whales in areas of the Pacific Ocean in 1999–2001. All samples were obtained by crossbow and comprised both epidermis and subcutaneous blubber. To evaluate exposure, 7 carcinogenic PAHs were analyzed in lipids extracted from Pacific Ocean sperm whale blubber, pooled by sex, and location. To evaluate PAH-DNA damage, portions of all tissue samples were formalin-fixed, paraffin-embedded, sectioned, and examined for PAH-DNA adducts by immunohistochemistry (IHC) using an antiserum elicited against benzo[a]pyrene-modified DNA, which crossreacts with several high molecular weight carcinogenic PAHs bound to DNA. The IHC showed widespread epidermal nuclear localization of PAH-DNA adducts in the Gulf of Mexico whales (n = 15) but not in the Pacific Ocean whales (n = 4). A standard semiquantitative scoring system revealed significantly higher PAH-DNA adducts in the Gulf of Mexico whales compared to the whales from the Pacific Ocean study (p = .0002).
