Chemical kinetics

By Miss.Sejal Jethva

Reaction rate tends to increase with concentration – a phenomenon explained by collision theory.

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Chemical kinetics, also known as reaction kinetics, is the study of rates of chemical processes. Chemical kinetics includes investigations of how different experimental conditions can influence the speed of a chemical reaction and yield information about the reaction's mechanism and transition states, as well as the construction of mathematical models that can describe the characteristics of a chemical reaction. In 1864, Peter Waage and Cato Guldberg pioneered the development of chemical kinetics by formulating the law of mass action, which states that the speed of a chemical reaction is proportional to the quantity of the reacting substances.
Chemical kinetics deals with the experimental determination of reaction rates from which rate laws and rate constants are derived. Relatively simple rate laws exist for zero-order reactions (for which reaction rates are independent of concentration), first-order reactions, and second-order reactions, and can be derived for others. In consecutive reactions, the rate-determining step often determines the kinetics. In consecutive first-order reactions, a steady state approximation can simplify the rate law. The activation energy for a reaction is experimentally determined through the Arrhenius equation and the Eyring equation. The main factors that influence the reaction rate include: the physical state of the reactants, the concentrations of the reactants, the temperature at which the reaction occurs, and whether or not any catalysts are present in the reaction.

Contents

• 1 Factors affecting reaction rate
  • 1.1 Nature of the reactants
  • 1.2 Physical state
  • 1.3 Concentration
  • 1.4 Temperature
  • 1.5 Catalysts
  • 1.6 Pressure
• 2 Equilibrium
• 3 Free energy
• 4 Applications
• 5 See also
• 6 References
• 7 External links

Factors affecting reaction rate

Nature of the reactants

Depending upon what substances are reacting, the reaction rate varies. Acid/base reactions, the formation of salts, and ion exchange are fast reactions. When covalent bond formation takes place between the molecules and when large molecules are formed, the reactions tend to be very slow. Nature and strength of bonds in reactant molecules greatly influence the rate of its transformation into products.

Physical state

The physical state (solid, liquid, or gas) of a reactant is also an important factor of the rate of change. When reactants are in the same phase, as in aqueous solution, thermal motion brings them into contact. However, when they are in different phases, the reaction is limited to the interface between the reactants. Reaction can occur only at their area of contact; in the case of a liquid and a gas, at the surface of the liquid. Vigorous shaking and stirring may be needed to bring the reaction to completion. This means that the more finely divided a solid or liquid reactant the greater its surface area per unit volume and the more contact it makes with the other reactant, thus the faster the reaction. To make an analogy, for example, when one starts a fire, one uses wood chips and small branches — one does not start with large logs right away. In organic chemistry, on water reactions are the exception to the rule that homogeneous reactions take place faster than heterogeneous reactions.

Concentration

The reactions are due to collisions of reactant species. The frequency with which the molecules or ions collide depends upon their concentrations. The more crowded the molecules are, the more likely they are to collide and react with one another. Thus, an increase in the concentrations of the reactants will result in the corresponding increase in the reaction rate, while a decrease in the concentrations will have a reverse effect. For example, combustion that occurs in air (21% oxygen) will occur more rapidly in pure oxygen.

Temperature

Temperature usually has a major effect on the rate of a chemical reaction. Molecules at a higher temperature have more thermal energy. Although collision frequency is greater at higher temperatures, this alone contributes only a very small proportion to the increase in rate of reaction. Much more important is the fact that the proportion of reactant molecules with sufficient energy to react (energy greater than activation energy: E > E_a) is significantly higher and is explained in detail by the Maxwell–Boltzmann distribution of molecular energies.
The 'rule of thumb' that the rate of chemical reactions doubles for every 10 °C temperature rise is a common misconception. This may have been generalized from the special case of biological systems, where the α (temperature coefficient) is often between 1.5 and 2.5.
A reaction's kinetics can also be studied with a temperature jump approach. This involves using a sharp rise in temperature and observing the relaxation time of the return to equilibrium. A particularly useful form of temperature jump apparatus is a shock tube, which can rapidly jump a gas's temperature by more than 1000 degrees.

Catalysts

Generic potential energy diagram showing the effect of a catalyst in a hypothetical endothermic chemical reaction. The presence of the catalyst opens a different reaction pathway (shown in red) with a lower activation energy. The final result and the overall thermodynamics are the same.

A catalyst is a substance that accelerates the rate of a chemical reaction but remains chemically unchanged afterwards. The catalyst increases rate reaction by providing a different reaction mechanism to occur with a lower activation energy. In autocatalysis a reaction product is itself a catalyst for that reaction leading to positive feedback. Proteins that act as catalysts in biochemical reactions are called enzymes. Michaelis–Menten kinetics describe the rate of enzyme mediated reactions. A catalyst does not affect the position of the equilibria, as the catalyst speeds up the backward and forward reactions equally.
In certain organic molecules, specific substituents can have an influence on reaction rate in neighbouring group participation.
Agitating or mixing a solution will also accelerate the rate of a chemical reaction, as this gives the particles greater kinetic energy, increasing the number of collisions between reactants and, therefore, the possibility of successful collisions.

Pressure

Increasing the pressure in a gaseous reaction will increase the number of collisions between reactants, increasing the rate of reaction. This is because the activity of a gas is directly proportional to the partial pressure of the gas. This is similar to the effect of increasing the concentration of a solution.
In addition to this straightforward mass-action effect, the rate coefficients themselves can change due to pressure. The rate coefficients and products of many high-temperature gas-phase reactions change if an inert gas is added to the mixture; variations on this effect are called fall-off and chemical activation. These phenomena are due to exothermic or endothermic reactions occurring faster than heat transfer, causing the reacting molecules to have non-thermal energy distributions (non-Boltzmann distribution). Increasing the pressure increases the heat transfer rate between the reacting molecules and the rest of the system, reducing this effect.
Condensed-phase rate coefficients can also be affected by (very high) pressure; this is a completely different effect than fall-off or chemical-activation. It is often studied using diamond anvils.
A reaction's kinetics can also be studied with a pressure jump approach. This involves making fast changes in pressure and observing the relaxation time of the return to equilibrium.

Equilibrium

While a chemical kinetics is concerned with the rate of a chemical reaction, thermodynamics determines the extent to which reactions occur. In a reversible reaction, chemical equilibrium is reached when the rates of the forward and reverse reactions are equal (the principle of detailed balance) and the concentrations of the reactants and products no longer change. This is demonstrated by, for example, the Haber–Bosch process for combining nitrogen and hydrogen to produce ammonia. Chemical clock reactions such as the Belousov–Zhabotinsky reaction demonstrate that component concentrations can oscillate for a long time before finally attaining the equilibrium.

Free energy

In general terms, the free energy change (ΔG) of a reaction determines whether a chemical change will take place, but kinetics describes how fast the reaction is. A reaction can be very exothermic and have a very positive entropy change but will not happen in practice if the reaction is too slow. If a reactant can produce two different products, the thermodynamically most stable one will in general form, except in special circumstances when the reaction is said to be under kinetic reaction control. The Curtin–Hammett principle applies when determining the product ratio for two reactants interconverting rapidly, each going to a different product. It is possible to make predictions about reaction rate constants for a reaction from free-energy relationships.
The kinetic isotope effect is the difference in the rate of a chemical reaction when an atom in one of the reactants is replaced by one of its isotopes.
Chemical kinetics provides information on residence time and heat transfer in a chemical reactor in chemical engineering and the molar mass distribution in polymer chemistry.

Applications

The mathematical models that describe chemical reaction kinetics provide chemists and chemical engineers with tools to better understand and describe chemical processes such as food decomposition, microorganism growth, stratospheric ozone decomposition, and the complex chemistry of biological systems. These models can also be used in the design or modification of chemical reactors to optimize product yield, more efficiently separate products, and eliminate environmentally harmful by-products. When performing catalytic cracking of heavy hydrocarbons into gasoline and light gas, for example, kinetic models can be used to find the temperature and pressure at which the highest yield of heavy hydrocarbons into gasoline will occur. Kinetics is also a basic aspect of chemistry.

See also

• Autocatalytic reactions and order creation
• Detonation
• Enthalpy
• Flame speed
• Nonthermal surface reaction
• PottersWheel Matlab toolbox to fit chemical rate constants to experimental data
• Reaction progress kinetic analysis
• Two-dimensional gas

References

• Preparing for the Chemistry AP Exam. Upper Saddle River, New Jersey: Pearson Education, 2004. 131–134. ISBN 0-536-73157-8

Electron pair

                                                                             By Miss Sejal D Jethva

In chemistry, an electron pair or a Lewis pair consists of two electrons that occupy the same orbital but have opposite spins. The electron pair concept was introduced in a 1916 paper of Gilbert N. Lewis.^[1]

MO diagrams depicting covalent (left) and polar covalent (right) bonding in a diatomic molecule. In both cases a bond is created by the formation of an electron pair.

Because electrons are fermions, the Pauli exclusion principle forbids these particles from having exactly the same quantum numbers. Therefore the only way to occupy the same orbital, i.e. have the same orbital quantum numbers, is to differ in the spin quantum number. This limits the number of electrons in the same orbital to exactly two.
The pairing of spins is often energetically favorable and electron pairs therefore play a very large role in chemistry. They can form

1. a chemical bond between two atoms
2. as a lone pair.
3. fill the core levels of an atom.

Because the spins are paired, the magnetic moment of the electrons cancels and the contribution of the pair to the magnetic properties will in general be a diamagnetic one.
Although a strong tendency to pair off electrons can be observed in chemistry, it is also possible that electrons occur as unpaired electrons.
In the case of metallic bonding the magnetic moments also compensate to a large extent, but the bonding is more communal so that individual pairs of electrons cannot be distinguished and it is better to consider the electrons as a collective 'ocean'.
A very special case of electron pair formation occurs in superconductivity: the formation of Cooper pairs.

Alkylating antineoplastic agent By Dr.Rajarshi N Patel & Mr.Dharam M Pandya

Alkylating antineoplastic agent

                                         Dr.Rajarshi N Patel & Mr.Dharam M Pandya

An alkylating antineoplastic agent is an alkylating agent used in cancer treatment that attaches an alkyl group (C_nH_2n+1) to DNA.^[1]
The alkyl group is attached to the guanine base of DNA, at the number 7 nitrogen atom of the purine ring.
Since cancer cells, in general, proliferate faster and with less error-correcting than healthy cells, cancer cells are more sensitive to DNA damage — such as being alkylated. Alkylating agents are used to treat several cancers. However, they are also toxic to normal cells (cytotoxic), leading to damage, in particular in cells that divide frequently, as those in the gastrointestinal tract, bone marrow, testicles and ovaries, which can cause loss of fertility. Most of the alkylating agents are also carcinogenic. Hyperthermia is especially effective at enhancing the effects of alkylating agents.^[2]

Contents

• 1 History
• 2 Agents acting nonspecifically
• 3 Agents requiring activation
• 4 Dialkylating agents, limpet attachment, and monoalkylating agents
• 5 Examples
  • 5.1 Classical alkylating agents
  • 5.2 Alkylating-like
  • 5.3 Nonclassical
• 6 Limitations
• 7 References
• 8 External links

History

Before their use in chemotherapy, alkylating agents were better known for their use as sulfur mustard, ("mustard gas") and related chemical weapons in World War I. The nitrogen mustards were the first alkylating agents used medically, as well as the first modern cancer chemotherapies. Goodman, Gilman, and others at Yale began studying nitrogen mustards at Yale in 1942, and, following the sometimes dramatic but highly variable responses of experimental tumors in mice to treatment, these agents were first tested in humans late that year. Use of methyl bis (B-chloroethyl)emine hydrochloride (mechlorethamine, mustine) and tris (B-chloroethy) amine hydrochloride for Hodgkin's disease lymphosarcoma, leukemia, and other malignancies resulted in striking but temporary dissolution of tumor masses. Because of secrecy surrounding the war gas program, these results were not published until 1946.^[3] These publications spurred rapid advancement in the previously non-existent field of cancer chemotherapy, and a wealth of new alkylating agents with therapeutic effect were discovered over the following two decades.^[4]
A common myth holds that Goodman and Gilman were prompted to study nitrogen mustards as a potential treatment for cancer following a 1943 incident in Bari, Italy, where survivors exposed to mustard gas became leukopenic. In fact, animal and human trials had begun the previous year, Gilman makes no mention of such an episode in his recounting of the early trials of nitrogen mustards,^[5] and the marrow suppressing effects of mustard gas had been known since the close of World War I.^[4]

Agents acting nonspecifically

Some alkylating agents are active under conditions present in cells; and the same mechanism that makes them toxic allows them to be used as anti-cancer drugs. They stop tumor growth by crosslinking guanine nucleobases in DNA double-helix strands, directly attacking DNA. This makes the strands unable to uncoil and separate. As this is necessary in DNA replication, the cells can no longer divide. These drugs act nonspecifically.

Agents requiring activation

Some of the substances require conversion into active substances in vivo (e.g., cyclophosphamide).
Cyclophosphamide is one of the most potent immunosuppressive substances. In small dosages, it is very efficient in the therapy of systemic lupus erythematosus, autoimmune hemolytic anemias, Wegener's granulomatosis, and other autoimmune diseases. High dosages cause pancytopenia and hemorrhagic cystitis.

Dialkylating agents, limpet attachment, and monoalkylating agents

Dialkylating agents can react with two different 7-N-guanine residues, and, if these are in different strands of DNA, the result is cross-linkage of the DNA strands, which prevents uncoiling of the DNA double helix. If the two guanine residues are in the same strand, the result is called limpet attachment of the drug molecule to the DNA. Busulfan is an example of a dialkylating agent: it is the methanesulfonate diester of 1,4-butanediol. Methanesulfonate can be eliminated as a leaving group. Both ends of the molecule can be attacked by DNA bases, producing a butylene crosslink between two different bases.
Monoalkylating agents can react only with one 7-N of guanine.
Limpet attachment and monoalkylation do not prevent the separation of the two DNA strands of the double helix but do prevent vital DNA-processing enzymes from accessing the DNA. The final result is inhibition of cell growth or stimulation of apoptosis, cell suicide.

Examples

In the Anatomical Therapeutic Chemical Classification System, alkylating agents are classified under L01A.

Classical alkylating agents

Many of the agents are known as "Classical alkylating agents". These include true alkyl groups, and have been known for a longer time than some of the other alkylating agents. Examples include melphalan and chlorambucil.^[6]
They destroy proliferating cancer cells by adding an alkyl group to DNA molecule and preventing its replication.
The following three groups are almost always considered "classical".

• Nitrogen mustards^[7]
  • Cyclophosphamide
  • Mechlorethamine or mustine (HN2) (trade name Mustargen)
  • Uramustine or uracil mustard
  • Melphalan
  • Chlorambucil
  • Ifosfamide
  • Bendamustine

• Nitrosoureas
  • Carmustine
  • Lomustine
  • Streptozocin

• Alkyl sulfonates
  • Busulfan

Thiotepa and its analogues are usually considered classical, but can be considered nonclassical.

Alkylating-like

Platinum-based chemotherapeutic drugs (termed platinum analogues) act in a similar manner. These agents do not have an alkyl group, but nevertheless damage DNA.^[8] They permanently coordinate to DNA to interfere with DNA repair, so they are sometimes described as "alkylating-like".

• Platinum^[7]
  • Cisplatin
  • Carboplatin
  • Nedaplatin
  • Oxaliplatin
  • Satraplatin
  • Triplatin tetranitrate

These agents also bind at N7 of guanine.

Nonclassical

Certain alkylating agents are sometimes described as "nonclassical". There is not a perfect consensus on which items are included in this category, but, in general, they include:

• procarbazine^[9]

• altretamine^[10]

• Some sources explicitly exclude the tetrazines (dacarbazine, mitozolomide, temozolomide) from the nonclassical category.^[11] However, other sources list dacarbazine as nonclassical,^[12] and some include temozolomide.^[13]

• The platinum agents are also sometimes described as nonclassical.^[14]

Limitations

Alkylating antineoplastic agents have limitations. Their functionality has been found to be limited when in the presence of the DNA-repair enzyme O-6-methylguanine-DNA methyltransferase (MGMT). Cross-linking of double-stranded DNA by alkylating agents is inhibited by the cellular DNA-repair mechanism, MGMT. If the MGMT promoter region is methylated, the cells no longer produce MGMT, and are therefore more responsive to alkylating agents. Methylation of the MGMT promoter in gliomas is a useful predictor of the responsiveness of tumors to alkylating agents.^[15]

References

1. Jump up ^ "antineop". Archived from the original on 7 March 2009. Retrieved 2009-01-24.
2. Jump up ^ Wiedemann GJ, Robins HI, Gutsche S, Mentzel M, Deeken M, Katschinski DM, Eleftheriadis S, Crahé R, Weiss C, Storer B, Wagner T. (May 1996). "Ifosfamide, carboplatin and etoposide (ICE) combined with 41.8 degrees C whole body hyperthermia in patients with refractory sarcoma". European Journal of Cancer 32A (5): 888–92. PMID 9081372.
3. Jump up ^ Goodman LS, Wintrobe MM, Dameshek W, Goodman MJ, Gilman AZ, McLennan MT (1946). "Nitrogen mustard therapy". JAMA 132 (3): 126–132. doi:10.1001/jama.1946.02870380008004.
4. ^ Jump up to: ^{a b} Scott RB (1970). "Cancer chemotherapy--the first twenty-five years". Br Med J. 4 (5730): 259–265. doi:10.1136/bmj.4.5730.259. PMC 1819834. PMID 4319950.
5. Jump up ^ Gilman A (1963). "The initial clinical trial of nitrogen mustard". Am J Surg. 105 (5): 574–8. doi:10.1016/0002-9610(63)90232-0. PMID 13947966.
6. Jump up ^ McClean S, Costelloe C, Denny WA, Searcey M, Wakelin LP (June 1999). "Sequence selectivity, cross-linking efficiency and cytotoxicity of DNA-targeted 4-anilinoquinoline aniline mustards". Anticancer Drug Des. 14 (3): 187–204. PMID 10500495.
7. ^ Jump up to: ^{a b} Takimoto CH, Calvo E. "Principles of Oncologic Pharmacotherapy" in Pazdur R, Wagman LD, Camphausen KA, Hoskins WJ (Eds) Cancer Management: A Multidisciplinary Approach. 11 ed. 2008.
8. Jump up ^ Cruet-Hennequart S, Glynn MT, Murillo LS, Coyne S, Carty MP (April 2008). "Enhanced DNA-PK-mediated RPA2 hyperphosphorylation in DNA polymerase eta-deficient human cells treated with cisplatin and oxaliplatin". DNA Repair (Amst.) 7 (4): 582–96. doi:10.1016/j.dnarep.2007.12.012. PMID 18289945.
9. Jump up ^ Armand JP, Ribrag V, Harrousseau JL, Abrey L (June 2007). "Reappraisal of the use of procarbazine in the treatment of lymphomas and brain tumors". Ther Clin Risk Manag 3 (2): 213–24. doi:10.2147/tcrm.2007.3.2.213. PMC 1936303. PMID 18360630.
10. Jump up ^ Yasko, Joyce M.; Kirkwood, John M.; Lotze, Michael T. (1998). Current cancer therapeutics. Edinburgh: Churchill Livingstone. p. 3. ISBN 0-443-06527-6.
11. Jump up ^ Schmit-Neuerburg, Klaus-Peter; Reiner Labitzke (2000). Manual of Cable Osteosyntheses: History, Technical Basis, Biomechanics of the Tension Band Principle, and Instructions for Operation. Berlin: Springer. p. 166. ISBN 3-540-66508-0.
12. Jump up ^ Bailey, Christopher J.; Corner, Jessica (2001). Cancer nursing: care in context. Oxford: Blackwell Science. p. 214. ISBN 0-632-03998-1.
13. Jump up ^ Kutner, Jean S; Gonzales, Ralph (2006). Current Practice Guidelines in Primary Care: 2007 (Current Practice Guidelines in Primary Care). McGraw-Hill Professional. p. 118. ISBN 0-07-147781-0.
14. Jump up ^ Pizzo, Philip A.; Poplack, David G. (2006). Principles and practice of pediatric oncology. Hagerstown, MD: Lippincott Williams & Wilkins. p. 313. ISBN 0-7817-5492-5.
15. Jump up ^ N Engl J Med 2000;343;1350-4.