Zeus, check this out:
Pantothenic Acid: an Organ-Specific Pro-Oxidant Vitamin¶
"Coenzyme A is required for the initial activation of free fatty acids to fatty acyl-CoA thioesters prior to their oxidation or esterification to complex lipids 2,3. Consequently, it was expected that pantothenic acid deficiency would result in higher levels of free fatty acid in the liver, but not in the brain.
Surprisingly, however,
analysis of tissue docosahexaenoic acid revealed that dietary pantothenic acid deficiency decreased the brain levels of this fatty acid by 30%, while virtually abolishing it in the liver (Fig 2). This finding can be explained based on the fact that pantothenic acid is also a structural element of the acyl carrier protein which is an essential component of the fatty acid synthetase complex 1."
"
Pantothenic acid supplements to rats receiving pantothenic acid-deficient diet restored hepatic coenzyme A levels to control values (Fig 1), while
increasing liver DHA levels by about 50%, supporting the conclusion that fatty acid synthesis is more susceptible to pantothenic acid than is its oxidation/esterification."
"In our study, brain and liver neuroprostane levels in control rats were 32+-4 ng/g and 29+-/4 ng/g, respectively (Fig 2). In parallel to the impact of
pantothenic acid deficiency on tissue DHA, Pantothenic acid-deficient diet for 5 weeks did not change brain neuroprostane levels (Fig 2 ), while
dramatically decreasing hepatic levels by 70% (Fig 2)."
"Similar to their effects on liver DHA concentrations, pantothenic acid supplements to these rats partially restored hepatic neuroprostane concentrations (Fig 2) ["Neuroprostanes result from free radical-induced peroxidation of DHA 5. This fatty acid is the most easily oxidizable naturally-occurring fatty acid"]. Whether or not longer duration of PA supplements to rats receiving PA-deficient diet would have completely restored hepatic DHA and neuroprostanes to control levels remains to be investigated.
These data show that dietary deficiency of PA has profound effects on hepatic coenzyme A and DHA levels, while exerting minimal or no effect on these metabolites in the brain.
These organ-specific effects may be reflected in enhanced susceptibility of the liver to oxidative stress. This conclusion is evidenced by the diminished levels of neuroprostanes in livers of rats fed PA-deficient diet, coupled with undetectable changes in the brain levels of these sensitive markers of oxidative stress in the same rats."
"Animals and Diets
Male Sprague-Dawley rats (40-50 g; Sasco, Omaha, NE) were fed a PA-deficient diet (ICN Biomedicals, Costa Mesa, CA) for 5 weeks (PAD group), while control animals received regular rat chow for 5 weeks. Some rats receiving the PAD diet were supplemented with PA (100 mg/kg/d, orally) during the fifth week (PAD+PA group)."
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