Genotoxicity in child populations exposed to polycyclic aromatic hydrocarbons (PAHs) in the air from Tabasco, Mexico.

The economy of the state of Tabasco is based on oil extraction. However, this imposes major effects to the environment and communities. Examples are the Polycyclic Aromatic Hydrocarbons (PAHs) that may be found in the soil, water and sediment of the region. Their volatility makes them available to living beings and results in genotoxic activity. The purpose of this study was to quantify the levels of PAHs in the air at several points in the state, and to analyze their relationship with possible damage to DNA on local inhabitants. Single Cell Gel Electrophoresis Assay (Comet Assay) was applied to peripheral blood lymphocytes of five groups of children between six and 15 years of age. PAH samples were analyzed following US/EPA TO-13-A method. Results indicated the presence in the air of most of the 16 PAHs considered as high priority by EPA, some of which have been reported with carcinogenic activity. Differences (p<0.05) were found between PAHs concentration in the gaseous component and in the particulate component of air samples, with the greatest values for the gaseous component. Greatest PAH concentrations were detected in areas with high oil extraction activities. Children groups from high oil activity areas presented genotoxic damage labeled from moderate to high according to DNA migration from nuclei (Tail Length: 14.2 - 42.14 microm and Tail/Head: 0.97 - 2.83 microm) compared with control group (12.25 and 0.63 microm, respectively). The group with greatest cell damage was located in the area with the greatest oil activity. We conclude that the presence of PAHs in the air may represent a health risk to populations that are chronically exposed to them at high oil activity regions.

Charge movement and calcium currents in skeletal muscle fibers are enhanced by GTP gamma S.

G-proteins play several regulatory roles in the cell. They can modulate ionic channels directly or in association with second messengers. In skeletal muscle, G-proteins modulate the activity of calcium channels either by acting directly on the channel and/or through a cAMP-dependent phosphorylating mechanism. The activation of G-proteins by GTP gamma S can also induce force generation in skinned fibers. In this paper we studied the effect of GTP gamma S on charge movement and calcium currents (ICa) in rat and frog skeletal muscle, using the Vaseline gap technique. We observed an increase in both charge movement and ICa after the intracellular addition of 10-100 microM GTP gamma S. GDP beta S did not have any effect. Addition of protein kinase A catalytic subunit increased the ICa, probably through a phosphorylation process, but did not modify the charge movement. This suggests that protein kinase A and GTP gamma S are acting on different sites of the channel. It can be speculated that G-proteins may have a regulatory role in the excitation-contraction coupling mechanism by a direct effect on charge movement.

Effect of Ca2+ channel blockers on K+ contractures in twitch fibres of the frog (Rana pipiens).

1. The effects of Ca2+ channel blockers (nifedipine, nitrendipine and diltiazem) were tested on K+ contractures in single muscle fibres of the frog, Rana pipiens. 2. Nifedipine (1 microM) reduced the area under K+ contractures to 24 +/- 9% (4) (100 mM-K+) and 34 +/- 24% (4) (190 mM-K+). Nitrendipine (0.1 microM) reduced the area to 30 +/- 10% (4) (120 mM-K+). The blockade of the contractures was reversible. 3. Diltiazem (1 microM) shortened the first 190 mM-K+ contracture without affecting the peak amplitude. The first contractures, performed at 15-20 min after the removal of diltiazem, were greatly reduced to 29 +/- 14% (4). This effect was reversed after three to five contractures in the absence of the drug. Similar results were obtained with 60 and 100 mM-K+. 4. The resting potential in control saline and after a brief exposure to 120 mM-K+ was not affected by the dihydropyridines and diltiazem. 5. Slow and fast Ca2+ currents were not modified by 1 microM-diltiazem at any stimulation rate or with pre-pulse depolarizations. Diltiazem (50 microM) did not affect the fast Ca2+ current and reduced the slow one to 48 +/- 10% (4). 7. The reduction of K+ contractures by Ca2+ channel blocking agents was not related to a blockade of Ca2+ currents. This can be tentatively explained by interactions of these compounds on membranes sites which regulate the coupling between membrane depolarization and contraction.

Skeletal muscle Ca2+ channels.

Ca2+ channels are widely distributed among different cell types. We shall describe in this paper kinetic properties of voltage-dependent slow Ca2+ channels in mammalian and frog skeletal muscle fibres. In addition, recent data on a fast-activated Ca2+ channel will be presented. Finally, the possible physiological role of the channel will be considered.