Chlorine is a halogen (atomic weight 35.4527) with valences ranging from I to 7. Isotopes 35 (75.5%) and 37 (24.5%) occur naturally. Several artificial isotopes are radioactive. The chloride ton (CI ) is the most common chemical form in foods. The hypochlorous ion (CIO ) is produced endogenously in minute quantities for specific actions. 1 he pcrchlorate ion (CIO.,~ > is a synthetic compound with distinct biological activities. Organochlorme compounds (e.g. pesticides, herbicides, antibiotics, polychlorbiphenyls PCBs) will not be discussed here, since they enter the food supply only as contaminants.


CFTR cystic fibrosis transmembrane regulator (ABCC7) CLD congenital diarrhea gene (DRA, SLC26A3) NaCI sodium chloride, table salt

NKCC1 sodium/potassium-chioride transporter 1(SLC12A2) NKCC2 sodium/potassium-chloride transporter 2 (SLC12A1 )

Nutritional summary

Function: Chloride is the main anionic osmolyte in blood and extracellular iluid and contributes to active transpon of some nutrients and metabolites in intestines, kidney, and other tissues. Hydrochloric acid in stomach contributes to protein digestion and mactivation of ingested microorganisms. Immune cells use directed release ofhypochlorous acid to combat pathogens in blood and tissues.

Food sources: Meats, pickled foods, and sally snacks are the major chloride sources. Requirements: Intakes have to match chloride tosses. Under most situations a balance can be achieved with daily intakes ofa few hundred milligrams. Increased sweating (high with fever, heat, and high humidity) and diuresis can increase chloride needs to several grams per day. Very low chloride intake, for instance with fasting, can cause dizziness and weakness due to hypotension.

Excessive intake Higher than minimal chloride intakes may increase blood pressure, especially in genetically susceptible indiv iduals and when other hypertensive factors (such as obesity) arc present.

Dietary sources

Chloride intake closely correlates w ith sodium intake (Al-I3ander et ul.. 11, since most chloride comes from animal foods and added sail (NaCI). The chloride content of meat tends to correlate inversely with lai content. Plant-derived foods are uniformly low in chloride. Some salt substitutes, such as potassium chloride, can be minor sources. While the UK food composition tables contain data on chloride (UK food Standards Agency. 2001). US food composition databases lack this information.

Digestion and absorption

Large amounts of chloride arc secreted from the parietal cells ofthe stomach lining (as hydrochloric acid), pancreas, and the intestinal epithelium. Unstimulated, fasting gastric output is normally below 6mmolh. and can increase with stimulation to 13 25 mmol/h in healthy people. Chloride from these intestinal secretions and from dietary intakes is absorbed in small and large intestine nearly to completion. Absorption occurs by both passive diffusion and active transport.

Small intestine: As gastric acid enters the duodenum, its corrosive acidity must he neutralized and the chloride recovered, Transporters that secrete intracellular bicarbonate in exchange for luminal chloride achieve both at the same time. The dominant apical bicarbonato'chloride exchanger (Wang clal.. 2002) is the putative anion transporter 1 (PAT1, SLC26A6). Other transporters of this type may also be expressed, but play only a minor role, if any.

A much more limited amount of chloride is taken up during the absorption of some nutrients. Transport of catiotlic and neutral amino acids, carnitine, taurine, and beta-alanine by system B" requires the cotransport ofboth chloride and sodium (Nakanishi et al„ 2001). The transporter IMINO for proline and hydroxy proline also has an absolute chloride requirement. Other amino acid transporters show chloride conductance that is not directly coupled to their transport activity.

The chloride conductance regulator (cystic fibrosis transmembrane regulator. CFTR, ABCC7) at the luminal side of the small intestine is most important for the secretion of chloride tuto the small intestinal lumen, CFTR is both a chloride channel

Intestinal lumen

Brush border membrane

8 aso latera I

Capillary lumen

Capillary endothelium

Figur« It.S Inrrstinal chloride absorption and a regulator of the epithelial sodium channel and other ion transporters. Its activity is stimulated by cAMP-mediated phosphorylation. Since CF-TR is an ATP-binding cassette (ABC) transporter, it is energy- and magnesium-dependent. This gene is essential for normal chloride secretion in pancreas, lung epithelium, and other tissues. Relatively common variants impair ion transport control through as yet unknown mechanisms. Chloride follows its gradient across the basolateral membrane through sodium potassium-chloride transporters and chloride channels. An ABC transporter. cMOAT MRP2(ABCC2), which is closely related toCFTR and also activated by cAMP, regulates the chloride llow across the basolateral membrane (van Kutjck et at., 1996).

The tight junctions between the enteroeytes of the proximal intestines are relatively permeable for chloride ions, The chloride channel CIC2 has been located to the luminal side of the tight junctions (Mohammad-Panah et at,, 2(101 ). Paracellular diffusion across the tight junctions pro\ ides a chloride pathway unrelated toCFTR that can significantly contribute to chloride secretory capacity (Gyomorey et ul., 20(11 ). Large intestine: The luminal side of the colon enteroeytes contains a chloride/bicarbonate exchanger ( SLC26A3; llemmmki a at.. 1998), alternatively referred to as Cl T) (congenital diarrhea) and DR A (downregulated in adenoma). The sodium potassium-chloride transporter (NKCCt, SLC12A2) mediates chloride transport across the basolateral membrane in either direction as required.

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