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Term	Abbreviation	Description
Proton leak		Flux of protons driven by the protonmotive force across the inner mt-membrane, bypassing the ATP synthase and thus contributing to LEAK respiration. Proton leak-flux depends non-linearly (non-ohmic) on the protonmotive force. Compare: Proton slip.
Proton pump		Mitochondrial proton pumps are large enzyme complexes (CI, CIII, CIV, CV) spanning the inner mt-membrane, partially encoded by mtDNA. CI, CIII and CIV are proton pumps that drive protons against the electrochemical protonmotive force, driven by electron transfer from reduced substrates to oxygen. In contrast, ATP synthase (also known as CIV) is a proton pump that utilizes the energy of proton flow along the protonmotive force to drive phosphorylation of ADP to ATP.
Proton slip		Proton slip is a property of the proton pumps (Complexes CI, CIII, and CIV) when the proton slips back to the matrix side within the proton pumping process. Slip is different from the proton leak, which depends on Δp and is a property of the inner mt-membrane (including the boundaries between membrane-spanning proteins and the lipid phase). Slip is an uncoupling process that depends mainly on flux and contributes to a reduction in the biochemical coupling efficiency of ATP production and oxygen consumption. Together with proton leak and cation cycling, proton slip is compensated for by LEAK respiration or LEAK oxygen flux, L. Compare: Proton leak.
Q calibration - DatLab		Q calibration
Q-junction		The Q-junction is a junction for convergent electron flow in the Electron transfer pathway (ET-pathway) from type N substrates and mt-matrix dehydrogenases through Complex I (CI), from type F substrates and FA oxidation through electron-transferring flavoprotein Complex (CETF), from succinate (S) through Complex II (CII), from glycerophosphate (Gp) through glycerophosphate dehydrogenase Complex (CGpDH), from choline through choline dehydrogenase, from dihydro-orotate through dihydro-orotate dehydrogenase, and other enzyme Complexes into the Q-cycle (ubiquinol/ubiquinone), and further downstream to Complex III (CIII) and Complex IV (CIV). The concept of the Q-junction, with the N-junction and F-junction upstream, provides the rationale for defining Electron-transfer-pathway states and categories of SUIT protocols.
ROUTINE respiration	R	In the living cell, ROUTINE respiration (R) or ROUTINE activity in the physiological coupling state is controlled by cellular energy demand, energy turnover and the degree of coupling to phosphorylation (intrinsic uncoupling and pathological dyscoupling). The conditions for measurement and expression of respiration vary (oxygen flux in state R, J_O₂R or oxygen flow in state R, I_O₂R). If these conditions are defined and remain consistent within a given context, then the simple symbol R for respiratory state can be used to substitute the more explicit expression for respiratory activity. R and growth of cells is supported by exogenous substrates in culture media. In media without energy substrates, R depends on endogenous substrates. R cannot be measured in permeabilized cells or isolated mitochondria. R is corrected for residual oxygen consumption (ROX), whereas R´ is the uncorrected apparent ROUTINE respiration or total cellular oxygen consumption of cells including ROX.
Respiratory acceptor control ratio	RCR	The respiratory acceptor control ratio (RCR) is defined as State 3/State 4 [1]. If State 3 is measured at saturating [ADP], RCR is the inverse of the OXPHOS control ratio, L/P (when State 3 is equivalent to the OXPHOS state, P). RCR is directly but non-linearly related to the P-L control efficiency, j_P-L = 1-L/P, with boundaries from 0.0 to 1.0. In contrast, RCR ranges from 1.0 to infinity, which needs to be considered when performing statistical analyses. In living cells, the term RCR has been used for the ratio State 3u/State 4o, i.e. for the inverse L/E ratio [2,3]. Then for conceptual and statistical reasons, RCR should be replaced by the E-L coupling efficiency, 1-L/E [4].
Respiratory chain	RC	The mitochondrial respiratory chain (RC) consists of enzyme complexes arranged to form a metabolic system of convergent pathways for oxidative phosphorylation. In a general sense, the RC includes (1) the electron transfer pathway (ET-pathway), with transporters for the exchange of reduced substrates across the inner mitochondrial membrane, enzymes in the matrix space (particularly dehydrogenases of the tricarboxylic acid cycle), inner membrane-bound electron transfer complexes, and (2) the inner membrane-bound enzymes of the phosphorylation system.
Respiratory complexes	CI, CII, CIII, CIV, CETF, CGpDH, ..	Respiratory Complexes are membrane-bound enzymes consisting of several subunits which are involved in energy transduction of the respiratory system. » MiPNet article
Respiratory state		Respiratory states of mitochondrial preparations and living cells are defined in the current literature in many ways and with a diversity of terms. Mitochondrial respiratory states must be defined in terms of both, the coupling-control state and the electron-transfer-pathway state.
Respirometry		Respirometry is the quantitative measurement of respiration. Respiration is therefore a combustion, a very slow one to be precise (Lavoisier and Laplace 1783). Thus the basic idea of using calorimetry to explore the sources and dynamics of heat changes were present in the origins of bioenergetics (Gnaiger 1983). Respirometry provides an indirect calorimetric approach to the measurement of metabolic heat changes, by measuring oxygen uptake (and carbon dioxide production and nitrogen excretion in the form of ammonia, urea, or uric acid) and converting the oxygen consumed into an enthalpy change, using the oxycaloric equivalent. Liebig (1842) showed that the substrate of oxidative respiration was protein, carbohydrates, and fat. The sum of these chemical changes of materials under the influence of living cells is known as metabolism (Lusk 1928). The amount (volume STP) of carbon dioxide expired to the amount (volume STP) of oxygen inspired simultaneously is the respiratory quotient, which is 1.0 for the combustion of carbohydrate, but less for lipid and protein. Voit (1901) summarized early respirometric studies carried out by the Munich school on patients and healthy controls, concluding that the metabolism in the body was not proportional to the combustibility of the substances outside the body, but that protein, which burns with difficulty outside, metabolizes with the greatest ease, then carbohydrates, while fats, which readily burns outside, is the most difficultly combustible in the organism. Extending these conclusions on the sources of metabolic heat changes, the corresponding dynamics or respiratory control was summarized (Lusk 1928): The absorption of oxygen does not cause metabolism, but rather the amount of the metabolism determines the amount of oxygen to be absorbed. .. metabolism regulates the respiration.
STPD	STPD	At standard temperature and pressure dry (STPD: 0 °C = 273.15 K and 1 atm = 101.325 kPa = 760 mmHg), the molar volume of an ideal gas, V_m, and V_m,O₂ is 22.414 and 22.392 L∙mol^-1, respectively. Rounded to three decimal places, both values yield the conversion factor of 0.744 from units used in spiroergometry (V_O₂max [mL O₂·min^-1]) to SI units [µmol O₂·s^-1]. For comparison at normal temperature and pressure dry (NTPD: 20 °C), V_m,O₂ is 24.038 L∙mol^-1. Note that the SI standard pressure is 100 kPa, which corresponds to the standard molar volume of an ideal gas of 22.711 L∙mol^-1 and 22.689 L∙mol^-1 for O₂.
SUIT	SUIT	SUIT is the abbreviation for Substrate-Uncoupler-Inhibitor Titration. SUIT protocols are used with mt-preparations to study respiratory control in a sequence of coupling and pathway control states induced by multiple titrations within a single experimental assay. These studies use biological samples economically to gain maximum information with a minimum amount of cells or tissue.
SUIT-001	RP1
SUIT-001 O2 ce-pce D003	RP1 ce-pce
SUIT-001 O2 ce-pce D004	RP1 ce-pce blood
SUIT-001 O2 mt D001	RP1 mt
SUIT-001 O2 pfi D002	RP1 pfi
SUIT-002	RP2
SUIT-002 O2 ce-pce D007	RP2 ce-pce
SUIT-002 O2 ce-pce D007a	RP2 ce-pce blood
SUIT-002 O2 mt D005	RP2 mt
SUIT-002 O2 pfi D006	RP2 pfi
SUIT-003	CCP-ce
SUIT-003 AmR ce D058	AmR effect on ce
SUIT-003 AmR ce D059	AmR effect on ce - control
SUIT-003 Ce1;ce1P;ce3U;ce4Glc;ce5M;ce6Rot;ce7S;1Dig;1c;2Ama;3AsTm;4Azd	cePMGlc,S
SUIT-003 Ce1;ce2U-	ce
SUIT-003 Ce1;ce3U-	ce
SUIT-003 O2 ce D009	CCP-ce short
SUIT-003 O2 ce D012	CCP-ce(P)
SUIT-003 O2 ce D028	CCP-ce S permeability test
SUIT-003 O2 ce D037	CCP-ce Crabtree_R
SUIT-003 O2 ce D038	CCP-ce Crabtree_E
SUIT-003 O2 ce D039	CCP-ce microalgae
SUIT-003 O2 ce D050	CCP-ce Snv
SUIT-003 O2 ce D060	CCP-ce Snv,Mnanv
SUIT-003 O2 ce D061	CCP-ce Snv,Mnanv - control
SUIT-003 O2 ce D062	CCP-ce Snv - control
SUIT-003 O2 ce-pce D013	CCVP-Glc,M
SUIT-003 O2 ce-pce D018	CCVP-Glc
SUIT-003 O2 ce-pce D020	CCVP
SUIT-003 pH ce D067	CCP-Crabtree with glycolysis inhibition
SUIT-004	RP1-short
SUIT-004 O2 pfi D010	RP1-short pfi
SUIT-005	RP2-short
SUIT-005 O2 pfi D011	RP2-short pfi
SUIT-006	CCP-mtprep
SUIT-006 O2 ce-pce D029	CCP ce-pce PM
SUIT-006 O2 mt D022	CCP mt S(Rot)
SUIT-006 O2 mt D047	CCP mt PM
SUIT-006 Q ce-pce D073	CCP ce-pce S(Rot)
SUIT-006 Q mt D071	CCP mt S(Rot)
SUIT-007	Glutamate anaplerosis
SUIT-007 O2 ce-pce D030	Glutamate anaplerotic pathway
SUIT-008	PM+G+S_OXPHOS+Rot_ET
SUIT-008 O2 ce-pce D025	Q-junction ce-pce
SUIT-008 O2 mt D026	Q-junction mtprep
SUIT-008 O2 pce D25	NS(PGM)
SUIT-008 O2 pfi D014
SUIT-009 O2 ce-pce D016
SUIT-009 O2 mt D015
SUIT-010	Digitonin test
SUIT-010 O2 ce-pce D008	Dig titration-pce
SUIT-011	GM+S_OXPHOS+Rot_ET
SUIT-011 O2 pfi D024	NS physiological maximum capapcity in fibres
SUIT-012	PM+G_OXPHOS
SUIT-012 O2 ce-pce D052	N(PGM)
SUIT-012 O2 mt D027	N CCP mtprep
SUIT-013 AmR ce D023	O_{2 dependence of H₂O₂ production ce}
SUIT-014	GM+P+S_OXPHOS+Rot_ET
SUIT-014 O2 pfi D042	NS(PGM)
SUIT-015	F+G+P+S_OXPHOS+Rot_ET
SUIT-015 O2 pti D043	FNS(Oct,PGM)
SUIT-016	F+G+S+Rot_OXPHOS+Omy
SUIT-016 O2 pfi D044	FNS(Oct,GM)
SUIT-017	F+G+S_OXPHOS+Rot_ET
SUIT-017 O2 mt D046	FNS(Oct,GM)
SUIT-017 O2 pfi D049	FNS(Oct,GM)
SUIT-018 O2 mt D054
SUIT-019	Pal+Oct+P+G_OXPHOS+S+Rot_ET
SUIT-019 O2 pfi D045	FNS(PalOct,PGM)
SUIT-020	PM+G+S+Rot_OXPHOS+Omy
SUIT-020 O2 mt D032	Q-junction additivity and respiratory control for membrane potential
SUIT-021	OXPHOS (GM+S+Rot+Omy)
SUIT-021 O2 mt D035	NS(GM)
SUIT-022	AOX (ce CN+SHAM)
SUIT-022 O2 ce D051	AOX-ce CN+SHAM
SUIT-023	AOX-ce SHAM+CN
SUIT-023 O2 ce D053	AOX-ce SHAM+CN
SUIT-024	ATPase (PM)
SUIT-024 O2 ce-pce D056	N(PM)
SUIT-025	OXPHOS (F+M+P+G+S+Rot)
SUIT-025 O2 mt D057	FNS(Oct,PGM)
SUIT-027	Malate anaplerosis
SUIT-029 O2 mt D066	QC_imt_PM_T+OXPHOS+c+Omy_ET_G+S+Rot
SUIT-031	PM+S+Rot
SUIT-031 O2 ce-pce D079	PM+S+Rot
SUIT-031 O2 mt D075	PM+S+Rot
SUIT-031 Q ce-pce D074	PM+S+Rot

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