Question about NAC

IH,

I currently use Whey Isolate Protein powder in my diet everyday. I usually take anywhere from 4-6 scoops a day of it. Whey Isolate (and I think the lactoferin in it) is supposed to boost glutathione levels.

Would it be okay for me to drop NAC since I'm supplementing with the Whey Isolate or should I continue with it?

I'm running low on NAC so I wanted to make sure I wasn't overlapping/overdoing it with the way my diet is structured.

Thanks,

Hadrion

hadrion - From a glutathione standpoint, yes it would be a good replacement.

However, I'm not sure how it would compare in other areas. I've seen some interesting effects with say lipoic acid and NAC are taken together. But in anycase, it would probably work out. Glutathione is the main benefit.

NAC is cheap so I don't mind staying on it.

What were the studies indicating about NAC and ALA if you don't mind me asking?

You know I'm more concerned with overall health than just hair health, so I'm very interested.

hadrion - They reduce toxicity to lead, protect against ultraviolet radiation, the two in synergy protect against free-radicals generated from high glucose.

They also protect against potent estrogens such as 4-hydoxy estrogen and estradiol negative effects on DNA repair dysfunction.

While on this topic, here's a study I came across that might be of interest.

J Physiol Sci. 2007 Dec;57(6):343-8. Epub 2007 Nov 15.Click here to read Links
Effect of cysteine derivatives administration in healthy men exposed to intense resistance exercise by evaluation of pro-antioxidant ratio.
Zembron-Lacny A, Szyszka K, Szygula Z.

Department of Sport Medical Sciences, Faculty of Physical Culture, University of Physical Education Poznan, Gorzow Wlkp, Poland. agzem@gorzow.home.pl

The aim of this study was to ascertain the influence of cysteine derivatives on pro-antioxidant equilibrium and to compare the antioxidant effectiveness of N-acetylcysteine, alpha-lipoic acid, and taurine by using Loverro's coefficient (pro-antioxidant ratio) in healthy men exposed to intensity-resistance exercise. Fifty-five men were randomly assigned to one of four groups: control (CON, placebo), N-acetylcysteine (NAC 1.8 g.day(-1), 3 days), alpha-lipoic acid (LIP 1.2 g.day(-1), 3 days), or taurine (TAU 3 g.day(-1), 3 days). The erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activities, lipid peroxidation products (TBARS), and plasma protein thiol concentrations were evaluated. The P/A ratio was determined from the mean values of TBARS, SOD, GPx, and CAT. The applied exercise at maximal intensity induced the significant changes in pro-antioxidant equilibrium toward peroxidation, which was proved by a 25% increase in TBARS concentration in the CON group. The peroxidation was significantly diminished by NAC (-14%) and LIP (-16%), whereas TAU had no effect on the TBARS concentration. Cysteine derivatives administration prevented exercise-induced decline in SOD activity and increased in GPx activity during exercise. CAT activity changed only in the LIP group. The estimation of P/A ratio showed the lowest level of pro-antioxidant equilibrium after LIP administration. In the CON group, P/A ratio was directly correlated with the protein thiols level (r = 0.495, p < 0.001). These data confirm the antioxidant action of tested cysteine derivatives, particularly lipoic acid, and demonstrate the practical application of P/A ratio to evaluate the effectiveness of antioxidants in athletes.

And on a related study to the above question, here is an example of both NAC Lipoic acid used together:

J Alzheimers Dis. 2007 Sep;12(2):195-206.
Lipoic acid and N-acetyl cysteine decrease mitochondrial-related oxidative stress in Alzheimer disease patient fibroblasts.

In this study, we evaluated the effect of lipoic acid (LA) and N-acetyl cysteine (NAC) on oxidative [4-hydroxy-2-nonenal, N(epsilon)-(carboxymethyl)lysine and heme oxygenase-1] and apoptotic (caspase 9 and Bax) markers in fibroblasts from patients with Alzheimer disease (AD) and age-matched and young controls. AD fibroblasts showed the highest levels of oxidative stress, and the antioxidants, lipoic acid (1 mM) and/or N-acetyl cysteine (100 microM) exerted a protective effect as evidenced by decreases in oxidative stress and apoptotic markers. Furthermore, we observed that the protective effect of LA and NAC was more pronounced when both agents were present simultaneously. AD-type changes could be generated in control fibroblasts using N-methylprotoporphyrin to inhibit cytochrome oxidase assembly indicating that the the oxidative damage observed was associated with mitochondrial dysfunction. The effects of N-methylprotoporphyrine were reversed or attenuated by both lipoic acid and N-acetyl cysteine. These data suggest mitochondria are important in oxidative damage that occurs in AD. As such, antioxidant therapies based on lipoic acid and N-acetyl cysteine supplementation may be promising.

And here's a study of particular interest:

Biochem Biophys Res Commun. 2007 Nov 23;363(3):651-5.
Thiol supplementation inhibits metalloproteinase activity independent of glutathione status.

Matrix metalloproteinases (MMPs) are proteolytic enzymes that regulate both integrity and composition of the extracellular matrix (ECM). Excessive ECM breakdown by MMPs is implicated in many physiological and pathological conditions, such as atherosclerosis. Activated macrophages, especially in the atherosclerotic lesion, are a major source of reactive oxygen species (ROS). Antioxidants protect against ROS-induced MMPs activation and inhibit gelatinolytic activity. We sought to determine whether the antioxidants glutathione (GSH), N-acetylcysteine (NAC), or lipoic acid (LA) affect gelatinase production and secretion. The results show that thiol compounds affect MMPs expression and activity in different ways. MMP-2 activity is directly inhibited by NAC and GSH, while LA is ineffective. On the contrary, MMP-9 expression is inhibited by LA at a pretrascriptional level, and MMP-9 activity is stimulated by GSH through a direct interaction with the gelatinase itself. Although all thiols, these compounds have different properties and different cellular uptakes and metabolic characteristics, and this could explain, at least in part, their differential effects on MMPs.