1. animal cells swell when exposed to extracellular hypotonicity and shrink when exposed to extracellular hypertonicity.

However, cell swelling activates channels in the cell membrane that permit increased efflux of K+, Cl–, and small organic solutes referred to collectively as organic osmolytes. Water follows these osmotically active particles out of the cell, and the cell volum……………………………………………………………………………… 2………. Donnan and Gibbs showed that in the presence of a nondiffusible ion, the diffusible ions distribute themselves so that at equilibrium, their concentration ratios are equal:.

Cross-multiplying,

2.

This is the Gibbs–Donnan equation. It holds for any pair of cations and anions of the same valence. The Donnan effect on the distribution of ions has three effects in the body. First,

because of proteins (Prot–) in cells, there are more osmotically active particles in cells than in interstitial fluid, and since animal cells have flexible walls, osmosis would make them swell and eventually rupture if it were not for Na+–K+ adenosine triphosphatase (ATPase) pumping ions back out of cells (see below). Thus, normal cell volume and pressure depend on Na +–K+ ATPase. Second, because at equilibrium the distribution of permeant ions across the membrane (m in the example used here) is asymmetric, an electrical difference exists across the membrane whose magnitude can be determined by the Nernst equation (see below). In the example used here, side X will be negative relative to side Y. The charges line up along the membrane, with the concentration gradient for Cl– exactly balanced by the oppositely directed electrical gradient, and the same holds true for K +. Third, since there are more proteins in plasma than in interstitial fluid, there is a Donnan effect on ion movement across the capillary wall (see below). Chloride ions are present in higher concentration in the ECF than in the cell interior, and they tend to diffuse along this concentration gradient into the cell. The interior of the cell is negative relative to the exterior, and chloride ions are pushed out of the cell along this electrical gradient. An equilibrium is reached at which Cl– influx and Cl– efflux are equal. The membrane potential at which this equilibrium exists is the equilibrium potential. Its magnitude can be calculated from the Nernst equation, as follows:

0 K+ 150. The Na+–K+ pump is also electrogenicm MORPHOLOGY OF CELL .5 –90 Cl- 9.0 5. and at that equilibrium there is a slight excess of cations on the outside and anions on the insideThis condition is maintained by Na+–K+ ATPase.Where Table 1–2. which pumps K+ back into the cell and keeps the intracellular concentration of Na+ low.0 –70 Resting membrane potential = –70 Mv equilibrium is reached in which the tendency of K+ to move out of the cell is balanced by its tendency to move into the cell.0 Equilibrium Potential (mV) +60 15.0 125. Concentration (mmol/L of H2O) Ion Inside Cell Na + Outside Cell 150. Concentration of Some Ions Inside and Outside Mammalian Spinal Motor Neurons.

the lysosomes become engorged with the material the enzyme normally degrades. Proteins may be myristolated. attached to geranylgeranyl or farnesyl groups). the nuclei sediment first.3. This fraction includes organelles such as the ribosomes and peroxisomes. including a role in the regulation of apoptosis (see below). Proteins held by these glycosylphosphatidylinositol (GPI) anchors . The head end of the molecule contains the phosphate portion and is relatively soluble in water (polar. 5. . The enzyme complexes responsible for oxidative phosphorylation are lined up on the cristae • The enzyme complexes responsible for oxidative phosphorylation illustrate the Mitochondria have no effective DNA repair system. they are generally sausage-shaped (Figure 1–4).. When cells are homogenized and the resulting suspension is centrifuged. The uncharged. an intermembrane space. These include for the most part disorders of tissues with high metabolic rates in which energy production is defective as a result of abnormalities in the production of ATP. IN CELL MEMBRANThe major lipids are phospholipids such as phosphatidylcholine and phosphatidylethanolamine. sphingomyelin. and a central matrix space. hydrophilic portions are located on the surfaces. Each has an outer membrane. hydrophobic portions of the proteins are usually located in the interior of the membrane. they have specific lipids attached to them (Figure 1–6).000 times gravity or more causes a fraction made up of granules called the microsomes to sediment. ie. LYSOSOME When a lysosomal enzyme is congenitally absent. Over 40 GPIlinked cell surface proteins have now been described. the hydrophilic ends of the molecules are exposed to the aqueous environment that bathes the exterior of the cells and the aqueous cytoplasm. In the membrane. The tails are relatively insoluble (nonpolar. Mitochondria perform other functions. The shape of the phospholipid molecule is roughly that of a clothespin (Figure 1–5). palmitoylated. followed by the mitochondria. the membranes are relatively simple. hydrophobic). MITROCONDRIA. but oxidative phosphorylation is the most crucial. Other proteins are lipidated. an inner membrane.interactions between the products of the mitochondrial genome and the nuclear genome. 4. In mammals. In prokaryotes (cells such as bacteria in which there is no nucleus). and cholesterol. A large number of relatively rare diseases have now been traced to mutations in mitochondrial DNA. One common way is attachment to glycosylated forms of phosphatidylinositol. and the mutation rate for mitochondrial DNA is over 10 times the rate for nuclear DNA. . Peripheral proteins are attached to the surfaces of the membrane in various ways. which is folded to form shelves (cristae). whereas the charged. hydrophilic). or prenylated (ie. but in eukaryotes (cells containing nuclei). the hydrophobic ends meet in the water-poor interior of the membrane. Hundreds to thousands of mitochondria are in each eukaryotic cell. cell membranes contain various glycosphingolipids. High-speed centrifugation that generates forces of 100.

which causes mental retardation and blindness. —have been characterized. PPAR. -galactosidase A deficiency causes Fabry's disease. though their use in diabetes has been limited by their toxic side effects. which lower circulating triglycerides.'s.'s are activated by fasting and increase energy-producing enzyme activity.have received the most attention because PPAR. Three PPAR receptors— . which includes receptors for steroid hormones. When activated. Another example is the lysosomal storage disease called Tay–Sachs disease. Thiazolidinediones are synthetic ligands for PPAR. and a number of other substances (see below). certain vitamins. and .'s and they increase sensitivity to insulin.and PPAR. producing changes in the production of mRNAs. These receptors (PPARs) are members of the nuclear receptor superfamily.PEROXIZOME Peroxisomes are found in the microsomal fraction of cells . whereas PPAR. they bind to DNA. Fibrates. and galactocerebrosidase deficiency causes Gaucher's disease. but they are serious and can be fatal.'s are activated by feeding and initiate increases in enzymes involved in energy storage. thyroid hormones.This eventually leads to one of the lysosomal storage diseases. These diseases are rare. are ligands for PPAR. For example. • a number of synthetic compounds were found to cause proliferation of peroxisomes by acting on receptors in the nuclei of cells.