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Lifeforms concentrations of the categories of macromolecules, and Lipids

Lifeforms concentrations of the categories of macromolecules, and Lipids


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Lifeforms are formed of large, modular, organic molecules called macromolecules, large organic molecules called Lipids, and simpler molecules such as H2O.

Macromolecules are commonly grouped into the following categorises:

  • Protien
  • Nucleic Acid
  • Carbohydrate

The concentrations of these types of molecule by mass, in a dehydrated (therefore dead) "E. coli" are:

Protein: 55% Nucleic Acid: 23% Carbohydrate: 0% Lipid: 9%

From: http://book.bionumbers.org/what-is-the-macromolecular-composition-of-the-cell


Q: Repeating the above table for other lifeforms, for the whole organism if it is multi-cellular, can examples be given of lifeforms that are particular outliers?


I have been unable to find much more useful information, however this data probably exists, I could find nothing for larger lifeforms such an animals. Around 60% of a cells cytosol is proteins, however this is by volume, not by mass.


Macromolecule

A macromolecule is a very large molecule, such as a protein. They are composed of thousands of covalently bonded atoms. Many macromolecules are the polymerization of smaller molecules called monomers. The most common macromolecules in biochemistry are biopolymers (nucleic acids, proteins, and carbohydrates) and large non-polymeric molecules such as lipids and macrocycles. [1] Synthetic fibers and experimental materials such as carbon nanotubes [2] [3] are also examples of macromolecules.


Carbon

Universally known as the building block of life, carbon is arguably one of the most important elements on Earth. It receives this title because of a few important properties. The primary one being the ease with which it can bond with other elements. It can bond with adjacent atoms on all four sides as well as with other carbon atoms. These bonds are also very specific: strong enough to resist the environment, but weak enough for the body to control. This is thanks to carbon’s unique atomic structure. Each carbon is identical, having four electrons in its outer shell instead of the desirable eight. This is what allows it to bond to other atoms with such ease.

So what makes carbon so important to life? Most of the components of a cell are composed of four groups of macromolecules: carbohydrates, proteins, lipids, and nucleic acids (DNA/RNA). Carbohydrates serve as the main source of fuel for the body. The digestive track changes carbohydrates to glucose, which is then distributed throughout the body. Proteins do the majority of labor within cells. They also fight illnesses, carry out chemical reactions, and transmit signals. Lipids make up most of the non-protein part of cells. They are commonly known as fats, oils, vitamins, etc. The main function of nucleic acid (DNA/RNA) is to store and reproduce genetic material. Carbon truly is the building block of life. Without it, life would not exist.


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What are the types of lipid storage disease?

Gaucher disease is caused by a deficiency of the enzyme glucocerebrosidase. Fatty material can collect in the brain, spleen, liver, kidneys, lungs, and bone marrow. Symptoms may include brain damage, enlarged spleen and liver, liver malfunction, skeletal disorders and bone lesions that may cause pain and fractures, swelling of lymph nodes and (occasionally) adjacent joints, distended abdomen, a brownish tint to the skin, anemia, low blood platelets, and yellow spots in the eyes. Individuals affected most seriously may also be more susceptible to infection. The disease affects males and females equally.

Gaucher disease has three common clinical subtypes:

  • Type 1 (or nonneuronopathic type) is the most common form of the disease in the U.S. and Europe. The brain is not affected, but there may be lung and, rarely, kidney impairment. Symptoms may begin early in life or in adulthood and include enlarged liver and grossly enlarged spleen, which can rupture and cause additional complications. Skeletal weakness and bone disease may be extensive. People in this group usually bruise easily due to low blood platelet count. They may also experience fatigue due to anemia. Depending on disease onset and severity, individuals with type 1 may live well into adulthood. Many affected individuals have a mild form of the disease or may not show any symptoms. Although Gaucher type 1 occurs often among persons of Ashkenazi Jewish heritage, it can affect individuals of any ethnic background.
  • Type 2 (or acute infantile neuropathic Gaucher disease) typically begins within 3 months of birth. Symptoms include extensive and progressive brain damage, spasticity, seizures, limb rigidity, enlarged liver and spleen, abnormal eye movement, and a poor ability to suck and swallow. Affected children usually die before age 2.
  • Type 3 (the chronic neuronopathic form) can begin at any time in childhood or even in adulthood. It is characterized by slowly progressive but milder neurologic symptoms compared to the acute or type 2 Gaucher disease. Major symptoms include eye movement disorders, cognitive deficit, poor coordination, seizures, an enlarged spleen and/or liver, skeletal irregularities, blood disorders including anemia, and respiratory problems. Nearly everyone with type 3 Gaucher disease who receives enzyme replacement therapy will reach adulthood.

For type 1 and most type 3 individuals, enzyme replacement treatment given intravenously every two weeks can dramatically decrease liver and spleen size, reduce skeletal abnormalities, and reverse other manifestations. Successful bone marrow transplantation cures the non-neurological manifestations of the disease. However, this procedure carries significant risk and is rarely performed in individuals with Gaucher disease. Surgery to remove all or part of the spleen may be required on rare occasions (if the person has very low platelet counts or when the enlarged organ severely affects the person&rsquos comfort). Blood transfusion may benefit some anemic individuals. Others may require joint replacement surgery to improve mobility and quality of life. There is currently no effective treatment for the brain damage that may occur in people with types 2 and 3 Gaucher disease.

Niemann-Pick disease is a group of autosomal recessive disorders caused by an accumulation of fat and cholesterol in cells of the liver, spleen, bone marrow, lungs, and, in some instances, brain. Neurological complications may include ataxia (lack of muscle coordination that can affect walking steadily, writing, and eating, among other functions), eye paralysis, brain degeneration, learning problems, spasticity, feeding and swallowing difficulties, slurred speech, loss of muscle tone, hypersensitivity to touch, and some clouding of the cornea due to excess buildup of materials. A characteristic cherry-red halo that can be seen by a physician using a special tool develops around the center of the retina in 50 percent of affected individuals.

Niemann-Pick disease is subdivided into three categories:

  • Type A, the most severe form, begins in early infancy. Infants appear normal at birth but develop profound brain damage by 6 months of age, an enlarged liver and spleen, swollen lymph nodes, and nodes under the skin (xanthomas). The spleen may enlarge to as great as 10 times its normal size and can rupture, causing bleeding. These children become progressively weaker, lose motor function, may become anemic, and are susceptible to recurring infection. They rarely live beyond 18 months. This form of the disease occurs most often in Jewish families.
  • Type B (or juvenile onset) does not generally affect the brain but most children develop ataxia, damage to nerves exiting from the spinal cord (peripheral neuropathy), and pulmonary difficulties that progress with age. Enlargement of the liver and spleen characteristically occurs in the pre-teen years. Individuals with type B may live a comparatively long time but many require supplemental oxygen because of lung involvement. Niemann-Pick types A and B result from accumulation of the fatty substance called sphingomyelin, due to deficiency of an enzyme called sphingomyelinase.
  • Type C may appear early in life or develop in the teen or even adult years. Niemann-Pick disease type C is not caused by a deficiency of sphlingomyelinase but by a lack of the NPC1 or NPC2 proteins. As a result, various lipids and particularly cholesterol accumulate inside nerve cells and cause them to malfunction. Brain involvement may be extensive, leading to inability to look up and down, difficulty in walking and swallowing, progressive loss of hearing, and progressive dementia. People with type C have only moderate enlargement of their spleens and livers. Those individuals with Niemann-Pick type C who share a common ancestral background in Nova Scotia were previously referred to as type D. The life expectancies of people with type C vary considerably. Some individuals die in childhood while others who appear to be less severely affected can live into adulthood.

There is currently no cure for Niemann-Pick disease. Treatment is supportive. Children usually die from infection or progressive neurological loss. Bone marrow transplantation has been attempted in a few individuals with type B with mixed results.

Fabry disease, also known as alpha-galactosidase-A deficiency, causes a buildup of fatty material in the autonomic nervous system (the part of the nervous system that controls involuntary functions such as breathing and heart beat), eyes, kidneys, and cardiovascular system. Fabry disease is the only X-linked lipid storage disease. Males are primarily affected, although a milder and more variable form is common in females. Occasionally, affected females have severe manifestations similar to those seen in males with the disorder. Onset of symptoms is usually during childhood or adolescence. Neurological signs include burning pain in the arms and legs, which worsens in hot weather or following exercise, and the buildup of excess material in the clear layers of the cornea (resulting in clouding but no change in vision). Fatty storage in blood vessel walls may impair circulation, putting the person at risk for stroke or heart attack. Other symptoms include heart enlargement, progressive kidney impairment leading to renal failure, gastrointestinal difficulties, decreased sweating, and fever. Angiokeratomas (small, non-cancerous, reddish-purple elevated spots on the skin) may develop on the lower part of the trunk of the body and become more numerous with age.

People with Fabry disease often die prematurely of complications from heart disease, renal failure, or stroke. Drugs such as phenytoin and carbamazepine are often prescribed to treat pain that accompanies Fabry disease but do not treat the disease. Metoclopramide or Lipisorb (a nutritional supplement) can ease gastrointestinal distress that often occurs in people with Fabry disease, and some individuals may require kidney transplant or dialysis. Enzyme replacement can reduce storage, ease pain, and preserve organ function in some people with Fabry disease.

Farber&rsquos disease, also known as Farber&rsquos lipogranulomatosis, describes a group of rare autosomal recessive disorders that cause an accumulation of fatty material in the joints, tissues, and central nervous system. It affects both males and females. Disease onset is typically in early infancy but may occur later in life. Children who have the classic form of Farber&rsquos disease develop neurological symptoms within the first few weeks of life that may include increased lethargy and sleepiness, and problems with swallowing. The liver, heart, and kidneys may also be affected. Other symptoms may include joint contractures (chronic shortening of muscles or tendons around joints), vomiting, arthritis, swollen lymph nodes, swollen joints, hoarseness, and nodes under the skin which thicken around joints as the disease progresses. Affected individuals with breathing difficulty may require a breathing tube. Most children with the disease die by age 2, usually from lung disease. In one of the most severe forms of the disease, an enlarged liver and spleen can be diagnosed soon after birth. Children born with this form of the disease usually die within 6 months.

Farber's disease is caused by a deficiency of the enzyme called ceramidase. Currently there is no specific treatment for Farber&rsquos disease. Corticosteroids may be prescribed to relieve pain. Bone marrow transplants may improve granulomas (small masses of inflamed tissue) on people with little or no lung or nervous system complications. Older persons may have granulomas surgically reduced or removed.

The gangliosidoses are comprised of two distinct groups of genetic diseases. Both are autosomal recessive and affect males and females equally.

The GM1 gangliosidoses are caused by a deficiency of the enzyme beta-galactosidase, resulting in abnormal storage of acidic lipid materials particularly in the nerve cells in the central and peripheral nervous systems. GM1 gangliosidosis has three clinical presentations:

  • GM1 (the most severe subtype, with onset shortly after birth) may include neurodegeneration, seizures, liver and spleen enlargement, coarsening of facial features, skeletal irregularities, joint stiffness, distended abdomen, muscle weakness, exaggerated startle response, and problems with gait. About half of affected individuals develop cherry-red spots in the eye. Children may be deaf and blind by age 1 and often die by age 3 from either cardiac complications or pneumonia.
  • Late infantile GM1 gangliosidosis typically begins between ages 1 and 3 years. Neurological symptoms include ataxia, seizures, dementia, and difficulties with speech.
  • GM1 gangliosidosis develops between ages 3 and 30. Symptoms include decreased muscle mass (muscle atrophy), neurological complications that are less severe and progress at a slower rate than in other forms of the disorder, corneal clouding in some people, and sustained muscle contractions that cause twisting and repetitive movements or abnormal postures (dystonia). Angiokeratomas may develop on the lower part of the trunk of the body. The size of the liver and spleen in most affected individuals is normal.

The GM2 gangliosidoses also cause the body to store excess acidic fatty materials in tissues and cells, most notably in nerve cells. These disorders result from a deficiency of the enzyme beta-hexosaminidase. The GM2 disorders include:

  • Tay-Sachs disease (also known as GM2 gangliosidosis-variant B) and its variant forms are caused by a deficiency in the enzyme hexosaminidase A. The incidence has been particularly high among Eastern European and Ashkenazi Jewish populations, as well as certain French Canadians and Louisianan Cajuns. Affected children appear to develop normally for the first few months of life. Symptoms begin by 6 months of age and include progressive loss of mental ability, dementia, decreased eye contact, increased startle response to noise, progressive loss of hearing leading to deafness, difficulty in swallowing, blindness, cherry-red spots in the retina, and some paralysis. Seizures may begin in the child&rsquos second year. Children may eventually need a feeding tube and they often die by age 4 from recurring infection. No specific treatment is available. Anticonvulsant medications may initially control seizures. Other supportive treatment includes proper nutrition and hydration and techniques to keep the airway open. A rare form of the disorder, called late-onset Tay-Sachs disease, occurs in people in their 20s and early 30s and is characterized by unsteadiness of gait and progressive neurological deterioration.
  • Sandhoff disease (variant AB) is a severe form of Tay-Sachs disease. Onset usually occurs at the age of 6 months and is not limited to any ethnic group. Neurological signs may include progressive deterioration of the central nervous system, motor weakness, early blindness, marked startle response to sound, spasticity, shock-like or jerking of a muscle (myoclonus), seizures, abnormally enlarged head (macrocephaly), and cherry-red spots in the eye. Other symptoms may include frequent respiratory infections, heart murmurs, doll-like facial features, and an enlarged liver and spleen. There is no specific treatment for Sandhoff disease. As with Tay-Sachs disease, supportive treatment includes keeping the airway open and proper nutrition and hydration. Anti-seizure medications may initially control seizures. Children generally die by age 3 from respiratory infections.

Krabbe disease (also known as globoid cell leukodystrophy and galactosylceramide lipidosis) is an autosomal recessive disorder caused by deficiency of the enzyme galactocerebrosidase. The disease most often affects infants, with onset before age 6 months, but can occur in adolescence or adulthood. The buildup of undigested fats affects the growth of the nerve&rsquos protective insulating sheath (myelin sheath) and causes severe deterioration of mental and motor skills. Other symptoms include muscle weakness, reduced ability of a muscle to stretch (hypertonia), muscle stiffening (spasticity), sudden shock-like or jerking of the limbs (myoclonic seizures), irritability, unexplained fever, deafness, blindness, paralysis, and difficulty when swallowing. Prolonged weight loss may also occur. The disease may be diagnosed by enzyme testing and by identification of its characteristic grouping of cells into globoid bodies in the white matter of the brain, demyelination of nerves and degeneration, and destruction of brain cells. In infants, the disease is generally fatal before age 2. Individuals with a later onset form of the disease have a milder course of the disease and live significantly longer. No specific treatment for Krabbe disease has been developed, although early bone marrow transplantation may help some people.

Metachromatic leukodystrophy, or MLD, is a group of disorders marked by storage buildup in the white matter of the central nervous system and in the peripheral nerves and to some extent in the kidneys. Similar to Krabbe disease, MLD affects the myelin that covers and protects the nerves. This autosomal recessive disorder is caused by a deficiency of the enzyme arylsulfatase A. Both males and females are affected by this disorder.

MLD has three characteristic forms: late infantile, juvenile, and adult.

  • Late infantile MLD typically begins between 12 and 20 months following birth. Infants may appear normal at first but develop difficulty in walking and a tendency to fall, followed by intermittent pain in the arms and legs, progressive loss of vision leading to blindness, developmental delays and loss of previously acquired milestones, impaired swallowing, convulsions, and dementia before age 2. Children also develop gradual muscle wasting and weakness and eventually lose the ability to walk. Most children with this form of the disorder die by age 5.
  • Juvenile MLD typically begins between ages 3 and 10. Symptoms include impaired school performance, mental deterioration, ataxia, seizures, and dementia. Symptoms are progressive with death occurring 10 to 20 years following onset.
  • Adult symptoms begin after age 16 and may include ataxia, seizures, abnormal shaking of the limbs (tremor), impaired concentration, depression, psychiatric disturbances and dementia. Death generally occurs within 6 to 14 years after onset of symptoms.

There is no cure for MLD. Treatment is symptomatic and supportive. Bone marrow transplantation may delay progression of the disease in some cases. Considerable progress has been made with regard to gene therapies in animal models of MLD and in clinical trials.

Wolman&rsquos disease, also known as acid lipase deficiency, is a severe lipid storage disorder that is usually fatal by age 1. This autosomal recessive disorder is marked by accumulation of cholesteryl esters (normally a transport form of cholesterol) and triglycerides (a chemical form in which fats exist in the body) that can build up significantly and cause damage in the cells and tissues. Both males and females are affected by this disorder. Infants are normal and active at birth but quickly develop progressive mental deterioration, enlarged liver and grossly enlarged spleen, distended abdomen, gastrointestinal problems, jaundice, anemia, vomiting, and calcium deposits in the adrenal glands, causing them to harden.

Another type of acid lipase deficiency is cholesteryl ester storage disease. This extremely rare disorder results from storage of cholesteryl esters and triglycerides in cells in the blood and lymph and lymphoid tissue. Children develop an enlarged liver leading to cirrhosis and chronic liver failure before adulthood. Children may also have calcium deposits in the adrenal glands and may develop jaundice late in the disorder.

Enzyme replacement for both Wolman&rsquos disease and cholesteryl ester storage disease is currently under active investigation.


Abstract

Antimicrobial peptides are one of the most promising classes of antibiotic agents for drug-resistant bacteria. Although the mechanisms of their action are not fully understood, many of them are found to interact with the target bacterial membrane, causing different degrees of perturbations. In this work, we directly observed that a short peptide disturbs membranes by inducing lateral segregation of lipids without forming pores or destroying membranes. Aurein 1.2 (aurein) is a 13-amino acid antimicrobial peptide discovered in the frog Litoria genus that exhibits high antibiotic efficacy. Being cationic and amphiphilic, it binds spontaneously to a membrane surface with or without charged lipids. With a small-angle neutron scattering contrast matching technique that is sensitive to lateral heterogeneity in membrane, we found that aurein induces significant lateral segregation in an initially uniform lipid bilayer composed of zwitterionic lipid and anionic lipid. More intriguingly, the lateral segregation was similar to the domain formed below the order–disorder phase-transition temperature. To our knowledge, this is the first direct observation of lateral segregation caused by a peptide. With quasi-elastic neutron scattering, we indeed found that the lipid lateral motion in the fluid phase was reduced even at low aurein concentrations. The reduced lateral mobility makes the membrane prone to additional stresses and defects that change membrane properties and impede membrane-related biological processes. Our results provide insights into how a short peptide kills bacteria at low concentrations without forming pores or destroying membranes. With a better understanding of the interaction, more effective and economically antimicrobial peptides may be designed.


Abstract

Polymer-coated liposomes, particularly poly(ethylene glycol) (PEG)-substituted liposomes, have emerged as long-circulating carrier systems for drug delivery and diagnostic purposes. A rapid synthesis of three different types of multifunctional lipids with structurally diverse hydrophilic, polyether-based architectures via one- or two-pot approaches is described. Architectural variation is achieved by the combination of different oxyanionic polymerization strategies and various glycidyl ether building units. Branched polyglycerol lipids have been prepared via cholesterol- or 1,2-bis-n-alkyl glyceryl ether-initiated, oxyanionic ring-opening polymerization (ROP) of protected glycidyl ethers and glycidol, respectively. In addition to these polyglycerol-based lipids, we describe the synthesis of multifunctional PEGs as the hydrophilic part of the lipid, which can be compared to conventional stealth lipids, but bear an adjustable number of hydroxyl functions within the PEG backbone. These lipids can be readily obtained by random copolymerization of ethylene oxide and protected glycidyl ethers, such as ethoxyethyl glycidyl ether (EEGE) and isopropylidene glyceryl glycidyl ether (IGG). Polydispersities Mw/Mn of the amphiphilic polyether structures were in the range of 1.04–1.2 for the linear structures and 1.1–1.6 for the hyperbranched lipids. Critical micelle concentrations (CMC) have been determined via the pyrene fluorescence method and were in the range of 1.4–40.7 mg/L, correlated to molecular weight and functionality of the polar polyether segment. Liposomes containing these hydroxy-functional lipids have been prepared via the membrane extrusion method and have been visualized by transmission electron microscopy (TEM) and cryo-TEM.


Biological membrane lipids

The three principal classes of lipids that form the bilayer matrix of biological membranes are glycerophospholipids, sphingolipids, and sterols (principally cholesterol). The most important characteristic of molecules in the first two groups is their amphipathic structure—well separated hydrophilic (polar) and hydrophobic (nonpolar) regions. Generally, their shape is elongated, with a hydrophilic end or head attached to a hydrophobic moiety by a short intervening region of intermediate polarity. Because of the segregation of polarity and nonpolarity, amphipathic molecules in any solvent will spontaneously form aggregates that minimize energetically unfavourable contacts (by keeping unlike regions of molecules apart) and maximize favourable contacts with the solvent (by keeping similar regions of molecules together). The molecular arrangement of the aggregate depends upon the solvent and the details of the amphipathic structure of the lipid.

In water, micelles formed by soaps (the sodium or potassium salts of fatty acids) are one such aggregate. The polar or hydrophilic portion of the soap molecules forms the surface of the micelle, while the hydrocarbon chains form its interior and are thus completely protected from the energetically unfavourable contact with water, as described in the section Fatty acids: Physical properties. Biological membrane lipids, however, do not form spherical micelles in water but instead form topologically closed lamellar (layered) structures. The polar heads of the component molecules form the two faces of the lamella, while the hydrophobic moieties form its interior. Each lamella is thus two molecules in thickness, with the long axis of the component molecules perpendicular to the plane of the bilayer.

Other types of aggregates are also formed in water by certain amphipathic lipids. For example, liposomes are artificial collections of lipids arranged in a bilayer, having an inside and an outside surface. The lipid bilayers form a sphere that can trap a molecule inside. The liposome structure can be useful for protecting sensitive molecules that are to be delivered orally.


Abstract

Artificial cells, particularly cell-sized liposomes, serve as tools to improve our understanding of the physiological conditions of living cells. However, such artificial cells typically contain a more dilute solution of biomacromolecules than that found in living cells (300 mg mL –1 ). Here, we reconstituted the intracellular biomacromolecular conditions in liposomes using hyperosmotic pressure. Liposomes encapsulating 80 mg mL –1 of macromolecules of BSA or a protein mixture extracted from Escherichia coli were immersed in hypertonic sucrose. The concentration of macromolecules in BSA-containing liposomes was increased in proportion to the initial osmotic pressure ratio between internal and external media. On the other hand, the concentration of the protein mixture in liposomes could be saturated to reach the physiological concentration of macromolecules in cells. Furthermore, membrane transformation after the hypertonic treatment differed between BSA- and protein mixture-containing liposomes. These results strongly suggested that the crowded environment in cells is different from that found in typical single-component systems.


Abstract

Most small molecule chemotherapeutics must cross one or more cellular membrane barriers to reach their biochemical targets. Owing to the relatively low solubility of chemotherapeutics in the lipid membrane environment, high doses are often required to achieve a therapeutic effect. The resulting systemic toxicity has motivated efforts to improve the efficiency of chemotherapeutic delivery to the cellular interior. Toward this end, liposomes containing lipids with cationic head groups have been shown to permeabilize cellular membranes, resulting in the more efficient release of encapsulated drugs into the cytoplasm. However, the high concentrations of cationic lipids required to achieve efficient delivery remain a key limitation, frequently resulting in toxicity. Toward overcoming this limitation, here, we investigate the ability of ternary lipid mixtures to enhance liposomal delivery. Specifically, we investigate the delivery of the chemotherapeutic, doxorubicin, using ternary liposomes that are homogeneous at physiological temperature but have the potential to undergo membrane phase separation upon contact with the cell surface. This approach, which relies upon the ability of membrane phase boundaries to promote drug release, provides a novel method for reducing the overall concentration of cationic lipids required for efficient delivery. Our results show that this approach improves the performance of doxorubicin by up to 5-fold in comparison to the delivery of the same drug by conventional liposomes. These data demonstrate that ternary lipid compositions and cationic lipids can be combined synergistically to substantially improve the efficiency of chemotherapeutic delivery in vitro.


Guide to Biochemistry

Guide to Biochemistry provides a comprehensive account of the essential aspects of biochemistry. This book discusses a variety of topics, including biological molecules, enzymes, amino acids, nucleic acids, and eukaryotic cellular organizations. Organized into 19 chapters, this book begins with an overview of the construction of macromolecules from building-block molecules. This text then discusses the strengths of some weak acids and bases and explains the interaction of acids and bases involving the transfer of a proton from an acid to a base. Other chapters consider the effectiveness of enzymes, which can be appreciated through the comparison of spontaneous chemical reactions and enzyme-catalyzed reactions. This book discusses as well structure and function of lipids. The final chapter deals with the importance and applications of gene cloning in the fundamental biological research, which lies in the preparation of DNA fragments containing a specific gene. This book is a valuable resource for biochemists and students.

Guide to Biochemistry provides a comprehensive account of the essential aspects of biochemistry. This book discusses a variety of topics, including biological molecules, enzymes, amino acids, nucleic acids, and eukaryotic cellular organizations. Organized into 19 chapters, this book begins with an overview of the construction of macromolecules from building-block molecules. This text then discusses the strengths of some weak acids and bases and explains the interaction of acids and bases involving the transfer of a proton from an acid to a base. Other chapters consider the effectiveness of enzymes, which can be appreciated through the comparison of spontaneous chemical reactions and enzyme-catalyzed reactions. This book discusses as well structure and function of lipids. The final chapter deals with the importance and applications of gene cloning in the fundamental biological research, which lies in the preparation of DNA fragments containing a specific gene. This book is a valuable resource for biochemists and students.


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