Catabolism and the Production of ATP (Chapter 2: pp. 88-102) I.

Overview: Three stages of oxidative breakdown of nutrient molecules (Figure 2- ! in "ower"oint#. $. %tage &: 'reakdown of macromolecules to subunits: (igestion. '. %tage 2: 'reakdown of subunits of acet)l-*o$: +l)col)sis and ,)ruvate (eh)drogenase *om"lex. 'eta-Oxidation of Fatt) $cids *. %tage -: Oxidation of $cet)l-*o$ to *O2 and .2O. ,roduction of /$(. and $T,. Takes "lace in mitochondria. 0lectron Trans"ort and Oxidative ,hos"hor)lation. II. $. +l)col)sis: &! ste"s (,anel 2-12 Fig. 2- ! in book#. +lucose 3 2$T, 3 2/$(3 > 2 ,)ruvates 3 2 /$(. 3 4 $T, &. &st Five %to"s: $T, energ) is invested and energ) content is rearranged as glucose is converted to 2 molecules of gl)ceraldeh)de --"hos"hate. 2. %te"s 5- : 2 +l)ceraldeh)de --"hos"hates are oxidi6ed and the energ) released is used to s)nthesi6e 2 $T, (substrate level "hos"hor)lation# and 2 /$(.. The /$(3 can be regenerated for gl)col)sis b) lactate deh)drogenase (anaerobic# or b) electron shuttles (aerobic#. -. %te"s 1-&!: 0nerg) is rearranged to create 2 high-energ) molecules (,0,# which are used to s)nthesi6e 2 more $T,s. Two ")ruvates are the final "roducts of gl)col)sis. '. %te"s 5- : Oxidation of +l)ceraldeh)de --,hos"hate and the Formation of $T, and /$(. (Figures 2- 2 and 2- -#. III. The Oxidation of ,)ruvate and Fatt) $cids to $cet)l-*o$. $. ,)ruvate (eh)drogenase *om"lex in 7atrix of 7itochondria: ,)ruvate 3 /$(3 3 *oen6)me $ > $cet)l *o$ 3 *Os 3 /$(. The $cet)l-*o$ "roduced enters the citric acid c)cle while the high-energ) electrons enter the electron trans"ort chain (Figure 2- 8#. '. 'eta-Oxidation of Fatt) $cids to $cet)l-*o$. It is a 4-ste" c)cle that takes "lace in matrix of mitochondria. 0ach turn of the c)cle "roduces an acet)l *o$2 and /$(.2 a F$(.22 and a fatt) acid shortened b) 2 carbons. The $cet)l-*o$s "roduced can enter the citric acid c)cle while the high-energ) electrons enter the electron trans"ort chain (Figure 2-1&#.

I9. *itric $cid *)cle (,anel 2-8 and Figure 2-12#: $cet)l-*o$ enters the citric acid c)cle. 1 ste"s inside the mitochondria. For ever) acet)l-*o$ that enters the c)cle2 2 *O2 leave the c)cle. - /$(.2 & F$(.22 and & +T, are "roduced "er turn of the c)cle. Therefore2 as 2 carbons are com"letel) oxidi6ed to 2 *Os2 much of the energ) released is stored in highenerg) electrons. *hemical bond energ) is converted to high-energ) electrons. 9. 0lectron Trans"ort *hain and $T, %)nthase: The high-energ) electrons are donated to the electron trans"ort chain2 which is "art of the inner membrane of the mitochondria. The electrons lose energ) as the) travel through a series of carriers to the final electron acce"tor2 O2. 7uch of this released energ) is used to translocate "rotons across the inner membrane to the intermembrane s"ace creating an electrochemical gradient. The energ) in high-energ) electrons is converted to gradient energ). The "rotons are allowed to reenter the mitochondria through $T, s)nthase2 which uses the energ) released to s)nthesi6e $T, from $(, and ,i. 0lectrochemical gradient energ) is converted to chemical bond energ) in the form of "hos"hoanh)dride bonds. The whole "rocess is called oxidative "hos"hor)lation. 9I. %torage forms of 0nerg): $. +l)cogen: +lucose can be stored in gl)cogen granules2 which are made of al"ha &24 and al"ha &25 linkages of glucose. :hen glucose is needed for metabolism it can be released from gl)cogen. ,lants store glucose in starch granules2 which have fewer al"ha &25 branch "oints (Figure 2- ;#. '. Fatt) $cids: Fatt) acids are stored in triac)lgl)cerol (T$+#. Three fatt) acids are linked via ester bonds to a gl)cerol to form neutral fat. T$+ molecules will form a li"id dro"let. <i"ases can h)drol)6e the ester bonds to liberate the fatt) acids for catabolism (Figs. 2- 1 and 2-1&#. 9II. /itrogen *)cle: /ucleotides and $mino $cids. :e get most of our nitrogen from our diet in the form of "rotein and nucleic acids. Organic nitrogen "asses from organism to organism so not much fixation of molecular nitrogen is needed. $ few microorganisms are ca"able of fixing molecular nitrogen. 9III. Organi6ation and =egulation of 7etabolism: 7etabolic "athwa)s do not go full s"eed all the time. *ertain en6)mes in each metabolic "athwa) are regulator) en6)mes that set the s"eed of the "athwa). These en6)mes ma) be modulated b) reversible "hos"hor)lation (covalent modification# or b) the concentration of certain metabolites (allosteric regulation#. In metabolism there are branch "oints where a given metabolite can "roceed into one of several "athwa)s. The regulator) en6)mes hel" determine how much of the metabolite will go into each "athwa).