Through the practical, it was possible to determine the effect of certain toxins on ciliary movement using paramecium as an organism model. As Figure 1 shows, all the toxins have a different effect on paramecium velocity and therefore on ciliary activity.
According to Fig. 1 paramecium speed is inversely proportional to time. After the addition of Ni2+ (toxin A) at approximately 0.1Mm (0.099), the velocity of paramecium decreased gradually until it fully stopped after 1800 seconds (Fig. 1). It suggests that Ni2+ has a gradual effect on the inhibition of cell motility. Larson and Satir (1991) suggest is could be because N2+ acts initially in the cell membrane and then directly on the axoneme (cilia structure). N2+ inhibits microtubule translocation by acting on 14S and 22S dynein ( motor proteins which activity cause bending movement). However, the research carried by Larson and Satir (1991) establish that the effect of Ni2+ is predominant on 14S dynein. This gradual effect on the inhibition of cilia in paramecium is also supported by Fig …show more content…
Referring to fig. 1, toxin C initially seems to have a similar effect to toxin A (Ni+2). Both toxins decrease paramecium activity in a similar trend after 900 seconds. However, after that, the velocity of paramecium under the effect of toxic C increased gradually and surprisingly it overcame the control standards (Fig 1.). Similarly, fig. 2 increase and decrease the number of stationary cells. The obtained results suggest that the substance C could have a reversible mechanism. It could be compared to the action of toxin A (Ni2+) which according to Larsen and Satin (1991) have this effect. Their research shows that after the exposure of paramecium to Ni2+ ciliary motility paralysis could be reversed in different ways, for instance, the addition of EDTA. This concept could be applied to toxin C as seems to follow this
According to Fig. 1 paramecium speed is inversely proportional to time. After the addition of Ni2+ (toxin A) at approximately 0.1Mm (0.099), the velocity of paramecium decreased gradually until it fully stopped after 1800 seconds (Fig. 1). It suggests that Ni2+ has a gradual effect on the inhibition of cell motility. Larson and Satir (1991) suggest is could be because N2+ acts initially in the cell membrane and then directly on the axoneme (cilia structure). N2+ inhibits microtubule translocation by acting on 14S and 22S dynein ( motor proteins which activity cause bending movement). However, the research carried by Larson and Satir (1991) establish that the effect of Ni2+ is predominant on 14S dynein. This gradual effect on the inhibition of cilia in paramecium is also supported by Fig …show more content…
Referring to fig. 1, toxin C initially seems to have a similar effect to toxin A (Ni+2). Both toxins decrease paramecium activity in a similar trend after 900 seconds. However, after that, the velocity of paramecium under the effect of toxic C increased gradually and surprisingly it overcame the control standards (Fig 1.). Similarly, fig. 2 increase and decrease the number of stationary cells. The obtained results suggest that the substance C could have a reversible mechanism. It could be compared to the action of toxin A (Ni2+) which according to Larsen and Satin (1991) have this effect. Their research shows that after the exposure of paramecium to Ni2+ ciliary motility paralysis could be reversed in different ways, for instance, the addition of EDTA. This concept could be applied to toxin C as seems to follow this