Methanol could become a major automotive fuel in the U.S., and its use may result in increased exposure of the public to methanol vapor. Nearly all of the available information on methanol toxicity in humans relates to the consequences of acute, rather than chronic, exposu res. Acute methanol toxicity evolves in a well-understood pattern and consists of an uncompensated metabolic acidosis with superimposed toxicity to the visual system. The toxic properties of methanol are rooted in the factors that govern both the conversion of methanol to formic acid and the subsequent metabolism of formate to carbon dioxide in the folate pathway. In short, the toxic syndrome sets in if formate generation continues at a rate that exceeds its rate of metabolism. Current evidence indicates that formate accumulation will not challenge the metabolic capacity of the folate pathway at the anticipated levels of exposu re to automotive methanol vapor.

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The effect of vitamin A deficiency on the response of splenic lymphocytes to mitogenic stimulation was determined in an experimental rat model. Male Lewis rats were divided into three groups. The ad libitum group (AL) was fed unlimited amounts of a vitamin A-supplemented diet. The vitamin A-deficient group (DEF) received a commercial vitamin A-free diet. The pair-fed group (PF) received a vitamin A-containing diet equivalent in amount to that consumed by the DEP group. During the early stages of vitamin A deficiency (determined by cessation of weight gain), the rats were killed and the isolated splenic lymphocytes subjected to mitogenic stimulation. Lymphocytes from DEF rats had one-third the transformation response to the mitogens Concanavalin A, Phytohemagglutinin and E. coli Lipopolysaccharide S of the AL and PF groups. When the DEF rats were supplemented with vitamin A, the transformation response returned to control values within 3 days. In addition to the alterations in the immune response, the DEF rats showed a marked leukopenia, a decrease in the number of circulating lymphocytes and an increase in the number of circulating neutrophils.

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The immune status of rats fed a vitamin A-deficient diet (-A) was studied before they reached the weight plateau (stage 1), during the first 5 d of the weight plateau (stage 2) and during late stages of vitamin A deficiency (stage 3). Compared to vitamin A-supplemented (+A) animals, there were no significant differences in the relative splenic weights during the early and later stages of deficiency, but the total yield of isolated splenocytes was lower in -A rats during stages 2 and 3. The weights of the cervical and mesenteric lymph nodes were higher during the later stages of deficiency. In the spleen, concanavalin A (Con A)-induced responses were significantly depressed in -A rats at all three stages of deficiency. In stages 2 and 3 splenic pokeweed mitogen (PWM) responses were lower in -A than in +A rats. There were no changes in lymph node responses in stage 1. The Con A and PWM-induced responses of cervical lymph nodes of -A animals were higher in stages 2 and 3. Mesenteric lymph node responses were also higher in -A rats in stage 3. The alterations in the transformation responses of -A rats could not be explained by changes in the relative proportions of T-cell subsets.

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The effect of the quality and quantity of dietary fats on the morphology and function of the immune system of Sprague-Dawley rats fed either 5% mixed fat, 24% saturated fat, 24% polyunsaturated fat, or 24% partially saturated fat was examined. After 2.5 months of dietary treatment high fat groups showed evidence of splenic hyperplasia, however, no consistent morphologic changes were seen in the mesenteric lymph nodes (MLN). Splenocytes from rats fed the 24% polyunsaturated fat diet were cultured in fetal bovine serum (FBS) and had a depressed lymphocyte transformation response, which persisted after 5 months of dietary treatment. Supplementing the culture medium with 10% rat serum altered the transformation response profile, but high fat serum did not have an immunosuppressive effect. MLN lymphocytes from rats fed the 24% partially saturated diet for 2.5 months had an enhanced response to concanavalin A; at five months the response was elevated in the groups fed saturated as well as partially saturated fat diets. These results suggest that the modulating effect of fat on the immune system depends on the duration of feeding, the type of fat consumed and the organ examined.

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