Cytotoxic Effects of the Atrazine Herbicide on Erythrocytes and Liver Damage in Lithobates spectabilis

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Abstract

In Mexico, atrazine is one of the herbicides most widely authorized and used in different irrigation districts. Atrazine is a herbicide that contaminates aquatic systems. Previous studies have shown that atrazine causes damage to red blood cells and liver tissue in different aquatic species, including abnormalities in melanomacrophages. However, more information on amphibians is needed, since most of these studies have been done on fish. Furthermore, no study has determined the effect of atrazine on species native to Mexico. Therefore, in this study, we asked what the effects of atrazine are on the erythrocytes and melanomacrophages of the liver in the male frog (Lithobates spectabilis). In the present study, we analyzed (1) the cytotoxicity of atrazine using the micronucleus test, (2) the area of melanomacrophage centers and the presence of melanin, and (3) the characterization of liver damage using histological techniques. Our results show that atrazine is cytotoxic to erythrocytes, increases the area of and melanin presence in melanomacrophage centers, and causes liver damage in male L. spectabilis. Therefore, hepatotoxicity and cytotoxicity are indicators of environmental stress. We suggest monitoring Mexico’s aquatic systems and further analyzing atrazine effects and other pollutants on native species.

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ATP-dependent mechanics of red blood cells.

Jean-François Joanny, Martin Lenz, Cécile Sykes … (2009)

Red blood cells are amazingly deformable structures able to recover their initial shape even after large deformations as when passing through tight blood capillaries. The reason for this exceptional property is found in the composition of the membrane and the membrane-cytoskeleton interaction. We investigate the mechanics and the dynamics of RBCs by a unique noninvasive technique, using weak optical tweezers to measure membrane fluctuation amplitudes with mus temporal and sub nm spatial resolution. This enhanced edge detection method allows to span over >4 orders of magnitude in frequency. Hence, we can simultaneously measure red blood cell membrane mechanical properties such as bending modulus kappa = 2.8 +/- 0.3 x 10(-19)J = 67.6 +/- 7.2 k(B)T, tension sigma = 6.5 +/- 2.1 x 10(-7)N/m, and an effective viscosity eta(eff) = 81 +/- 3.7 x 10(-3) Pa s that suggests unknown dissipative processes. We furthermore show that cell mechanics highly depends on the membrane-spectrin interaction mediated by the phosphorylation of the interconnection protein 4.1R. Inhibition and activation of this phosphorylation significantly affects tension and effective viscosity. Our results show that on short time scales (slower than 100 ms) the membrane fluctuates as in thermodynamic equilibrium. At time scales longer than 100 ms, the equilibrium description breaks down and fluctuation amplitudes are higher by 40% than predicted by the membrane equilibrium theory. Possible explanations for this discrepancy are influences of the spectrin that is not included in the membrane theory or nonequilibrium fluctuations that can be accounted for by defining a nonthermal effective energy of up to E(eff) = 1.4 +/- 0.1 k(B)T, that corresponds to an actively increased effective temperature.

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Red blood cell oxidative stress impairs oxygen delivery and induces red blood cell aging

Joy G Mohanty, Enika Nagababu, Joseph M. Rifkind (2014)

Red Blood Cells (RBCs) need to deform and squeeze through narrow capillaries. Decreased deformability of RBCs is, therefore, one of the factors that can contribute to the elimination of aged or damaged RBCs from the circulation. This process can also cause impaired oxygen delivery, which contributes to the pathology of a number of diseases. Studies from our laboratory have shown that oxidative stress plays a significant role in damaging the RBC membrane and impairing its deformability. RBCs are continuously exposed to both endogenous and exogenous sources of reactive oxygen species (ROS) like superoxide and hydrogen peroxide (H2O2). The bulk of the ROS are neutralized by the RBC antioxidant system consisting of both non-enzymatic and enzymatic antioxidants including catalase, glutathione peroxidase and peroxiredoxin-2. However, the autoxidation of hemoglobin (Hb) bound to the membrane is relatively inaccessible to the predominantly cytosolic RBC antioxidant system. This inaccessibility becomes more pronounced under hypoxic conditions when Hb is partially oxygenated, resulting in an increased rate of autoxidation and increased affinity for the RBC membrane. We have shown that a fraction of peroxyredoxin-2 present on the RBC membrane may play a major role in neutralizing these ROS. H2O2 that is not neutralized by the RBC antioxidant system can react with the heme producing fluorescent heme degradation products (HDPs). We have used the level of these HDP as a measure of RBC oxidative Stress. Increased levels of HDP are detected during cellular aging and various diseases. The negative correlation (p < 0.0001) between the level of HDP and RBC deformability establishes a contribution of RBC oxidative stress to impaired deformability and cellular stiffness. While decreased deformability contributes to the removal of RBCs from the circulation, oxidative stress also contributes to the uptake of RBCs by macrophages, which plays a major role in the removal of RBCs from circulation. The contribution of oxidative stress to the removal of RBCs by macrophages involves caspase-3 activation, which requires oxidative stress. RBC oxidative stress, therefore, plays a significant role in inducing RBC aging.